Sandhigata siravyadha sr

180
“A COMPREHENSIVE STUDY OF ANATOMICAL LOCATION OF SHAKHAGATA VEDHYA SIRA STHANAS IN PARTICULAR DISEASES” By Dr. R. Annapurna A dissertation submitted to the R R a a j j i i v v G G a a n n d d h h i i U U n n i i v v e e r r s s i i t t y y o o f f H H e e a a l l t t h h S S c c i i e e n n c c e e s s , , K K a a r r n n a a t t a a k k a a , , B B a a n n g g a a l l o o r r e e. In partial fulfillment of the requirements for the degree of AYURVEDA VACHASPATHI - M.D (AYURVEDA) In RACHANA SHAREERA POST GRADUATE DEPARTMENT OF RACHANA SHAREER N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR 2006 Co-Guide Dr. Chandrakant Halli BAMS, MS (Shalya Tantra) . Guide Prof. Dr. S.B. Kotur BAMS, MD (Rachana Shareera)

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A COMPREHENSIVE STUDY OF ANATOMICAL LOCATION OF SHAKHAGATA VEDHYA SIRA STHANAS IN PARTICULAR DISEASES, By Dr. R. Annapurna, POST GRADUATE DEPARTMENT OF RACHANA SHAREER N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR

Transcript of Sandhigata siravyadha sr

Page 1: Sandhigata siravyadha sr

“A COMPREHENSIVE STUDY OF ANATOMICAL LOCATION OF

SHAKHAGATA VEDHYA SIRA STHANAS IN PARTICULAR DISEASES”

By

Dr. R. Annapurna

A dissertation submitted to the

RRRaaajjjiiivvv GGGaaannndddhhhiii UUUnnniiivvveeerrrsssiiitttyyy ooofff HHHeeeaaalllttthhh SSSccciiieeennnccceeesss,,, KKKaaarrrnnnaaatttaaakkkaaa,,, BBBaaannngggaaalllooorrreee.

In partial fulfillment of the requirements for the degree of

AYURVEDA VACHASPATHI - M.D (AYURVEDA)

In

RACHANA SHAREERA

POST GRADUATE DEPARTMENT OF RACHANA SHAREER N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR

2006

Co-Guide Dr. Chandrakant Halli

BAMS, MS (Shalya Tantra)

.

Guide Prof. Dr. S.B. Kotur

BAMS, MD (Rachana Shareera)

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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE

N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR

POST GRADUATE DEPARTMENT

OF RACHANA SHAREER

Certificate by the guide

This is to certify that the dissertation entitled “A Comprehensive

Study on Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular

Diseases” is a bonafide literary research work done by Dr. R. Annapurna in

partial fulfillment of the requirement for the degree of Ayurveda Vachaspathi –

M.D (Ayurveda) in RACHANA SHAREER.

Date: Place: Bidar

Signature of the Guide Prof. Dr. S.B. Kotur

;BAMS, MD (Rachana Shareera) Professor Department of Rachana Shareera

NKJ Ayurvedic Medical College & PG Centre Bidar – 585403

Karnataka.

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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE

N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR

POST GRADUATE DEPARTMENT

OF RACHANA SHAREER

Endorsement by the HOD, Principal/Head of the institution

This is to certify that the dissertation entitled “A Comprehensive Study on

Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular

Diseases” is a bonafide literary research work done by Dr.R. Annapurna under

the guidance of Prof. Dr. S. B. Kotur, M D (Rachana Shareer), Professor

Department of Post Graduate Studies in Rachana Shareer, N. K. Jabshetty

Ayurvedic College And Post Graduate Centre, Bidar.

Seal and signature of the Principal Prof. Dr. S. B. Kotur

BAMS, MD (Rachana Shareer), NKJ Ayurvedic Medical College & PG Centre

Bidar – 585403 Karnataka

Date: Place: Bidar

Seal and signature of the HOD Prof. Dr. N. G. Mulimani

B.Sc.;BAMS, MD (Rachna Shareer) NKJ Ayurvedic Medical College & PG Centre

Bidar – 585403 Karnataka

Date: Place: Bidar

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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE

N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR

POST GRADUATE DEPARTMENT

OF RACHANA SHAREER

Declaration by the candidate

I here by declare that this dissertation/ thesis entitled “A Comprehensive

Study on Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular

Diseases” is a bonafide and genuine research work carried out by me under the

guidance of Prof. Dr. S.B. Kotur M.D (Rachana Shareer), Professor, PG

Department of Rachana Shareer.

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Date: Place: Bidar

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BANGALORE

N.K.J. AYURVEDIC MEDICAL COLLEGE

AND PG CENTRE, BIDAR

POST GRADUATE DEPARTMENT OF

RACHANA SHAREER

Copyright

Declaration by the candidate

I here by declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall declare the rights to preserve, use and disseminate this dissertation/

thesis in print or electronic format for academic/ research purpose.

Signature of the candidate Dr. R. Annapurna

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Date: Place: Bidar

Signature of the candidate Dr. R. Annapurna

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ACKNOWLEDGEMENT

It gives great pleasure in extending my deep sense of gratitude and hearty thanks to my esteemed

Guide Dr. S. B. KOTUR, M. D. (Rachana Shareera.), Prof, Department of P. G. Studies in Rachana

Shareera for his guidance, motivation and encouragement throughout the academic carrier which made me

for the completion of this research work successfully.

I sincerely thank Prof. Dr. Chandrakantha Halli M. S. (Shalya Tantra) for a support and

guidance. I would like to express my profound gratitude towards Prof. Dr. N. G. Mulimani M. D.

(Rachana Shareera.), H.O.D., Dept. of Post Graduate Studies in Rachana Shareera for his timely guidance

help and constant support. I express my holy gratitude to the Chairman and Office bearer of management

committee of ‘CHIDAMBAR SHIKSHANA SAMSTHE’ for giving the opportunity to pressure my

post graduation at this institution.

I take this opportunity to thank all the Post Graduate teaching staff of the institution. And Dr.

T. D. Ksheerasagar, Prof. GAMC Bangalore for his valuable guidance.

I express my sincere, love and gratitude to my batch-mates Dr. Jambagi, Dr. Giritammannavar,

Dr. Gangavathi and Dr. Patil, for their moral support.

I am highly indebted to Dr. A. I. Akki, Dr. S. S. Gangoor, Dr. V. S. Choudhari, Dr. Girish. K. J.,

Dr. Yadahalli, Dr. V. S. Hiremath, Dr. Nagnoor, Dr. Trishaila for the able guidance and inspiration given

at various stages of my work.

I sincerely appreciate the assistance received from librarian and non-teaching staff of this

institution during the course of my study.

I remember with respect my Husband Dr. S. M. Kudari, Asst. Prof. B.V.V.S Ayurvedic College

Bagalkot, for his inspiration and encouragement. I sincerely thank my father Shri. R. VISHWANATH

GOUD, and my mother Smt. R. NIRMALA and mother-in-law, SMT. SUSHILA KUDARI and

FAMILY for their profound and unending love. I am grateful to my brother Mr. R. Prabhu, Mr. R.

Mahesh for their unconditional support. I express great love towards my son SUJAY who has inspired me

by his cuteness and naughty activities. Last but not least I thank Mr. Vidyanand, Mr. Sudhir and Mr.

Sampath, Padma’s Internet Café for their timely co-operation. I offer my sincere apologies to any omission

in the above list and appeal to consider them as fortuitous.

Date : Dr.R. ANNAPURNA Place : Bidar

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LIST OF ABBREVIATIONS

Cha. Su. - Charaka Sutrasthana

Atharva - Atharvana Veda

Su. Sha - Sushruta Shareera

Su. Ni. - Sushruta Nidana

Su. Su. - Sushruta Sutrasthana

Su. Chi. - Sushruta Chikitsasthana

A. H. - Astanga Hridaya

A. S. - Astanga Sangraha

Bha. Pra. - Bhava Prakasha

Bhe. Sam. - Bhela Samhita

Note:- 1) Hindi Numbering for Shloka references

Arabic Numbering for Bibliography

2) Serial Numbers of Bibliograph is also a reference number of paragraph.

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Abstract

ABSTRACT

Background and Objectives :

The science of Ayurveda is well recognized system of medicine has unique

technique for harmonious living. Ayurveda possess a glorious past with extraordinarily

enriched documentation of medicinal literature. The science has been given holistic status

through out the ages.

Knowledge of Rachana Shareera is mandatory for a student of any system of

medicine. It is a vital subject in pre-clinical studies. The terms used by our ancient

Acharyas in context of Rachana Shareera appears to be vague for a causal observer and

leads to a lot of confusion among the student and teachers, as the concepts of Ayurveda

Shareera evolved 3000 years ago. Because of generation gap concepts appear to be

misinterpreted or not fully passed on to future generation. So we are in cross roads

whether to accept the concepts as it is or not. At this junction it is our moral responsibility

to take up such studies to understand the concepts clearly and to pass on knowledge to

younger generation. So the study taken up here is “A COMPREHENSIVE STUDY ON

ANATOMICAL LOCATION OF SHAKHAGATA VEDHYA SIRA STHANAS IN

PARTICULAR DISEASES” with objectives –

To provide literary information of “SIRA SHAREERA” and “SIRA VYADHA

VIDHI SHAREERA”, And to interpret Shakhagata Siravyadhana Sthanas, with

their clinical applicability.

Material and Methods :

Sources of Data :

A. Authoritative Ayurveedic texts like Brihatrayee and Laghutrayee.

B. Other allied literature like Veda and commentaries of Brihatrayees.

C. Modern medical literature on Anatomy

D. Published latest information from journals

E. Materials from internet.

Methods :

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Abstract

The present study is related to literary research. Classical texts, modern literature,

journals and internet information is collected, reviewed and critically analysed to fulfil

the objective of the study.

Raktamokshana :

Raktamokshana is one of the important parasurgical denoting letting of blood

outside the body. Different modalities of Raktamokshana are adopted according to Dosha

Avastha, Rakta Avastha and Atura Avastha. ‘Siravyadha’ is one of the type of

Raktamokshana by Shastravacharana. So as to explain its significance a stanza Su. Sha.

8/23 is sufficient.

Sushruta has given same importance of Dosha to Rakta also, where in many

places he has classified many diseases as Raktaja also. As there is specific line of

Shodhana Chikitsa in Vata, Pitta, Kapha, such as Basti, Virechana, Vamana, likewise

Siravyadha is often recommended as Shodhana Chikitsa. There is an universal rule that

always Prakupita Doshas are expelled from their neartest root, such as Basti in Vata,

Virechana in Pitta, Vamana in Kapha, in general Sameepastha Marga is selected for

Shodhana purpose. When we have reviewed Sushruta Shareera Sthana 8th Chapter, it is

surprising that selected sites are recommended for Siravyadha in particular diseases,

probably Adhisthana Sthanas of Vyadhi.

Of course, it appears surprising and vague, why Sushruta has mentioned

particular site for Siravyadha in different diseases.

Why can’t common site is selected in all diseases? is debatable. As Sushruta is

giving particular anatomical sites in individual diseases, there must be a relation between

disease condition and Siravydha particularly anatomical, physiological, and patho-

physiological. Here it is necessary to take-up such study where in we can trace out any

structural relation, patho-physiological relation between site and disease. So a

comprehensive study is done to locate particular Sira of Vydhana Sthana on the basis of

available literature of Dosha concepts, anatomical and pathological perspective. The

study is limited to upper and lower extremities.

Interpretation and Conclusion :

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Abstract

So as to fulfill the objectives, a therough review of literature and analysis is done

on the basis of anatomical, physiological and pathological grounds. As Siravydha is

significant line of treatment where Sushruta has mentioned Siras of particular site in

particular disease. So a creative and logical approach has been done to locate Siras of

Siravydha Sthanas in particular disease with pathophysiological interpretation. By the

present study it can be concluded that Sira means vein, Siravydha is effective modality of

treatment, Siravyadha Sthanas in particular diseases cannot be discarded.

Key Words :

Sira, , Vein, Rachana Shareera, Raktamokshana, Siravyadha, Venesection,

Phlebotomy

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CONTENTS Page No.

I. INTRODUCTION 1 - 2 II. OBJECTIVES 3

III. REVIEW OF LITERATURE

PART (A) - 1) Etymology of Sira 4 2) Sirashareera 5 - 11 3) Critics of the term Sira and Dhamani 12 - 14

4) Raktamokshana vidhi 15 - 16

5) Siravyadhavidhi 17 - 23

6) Roganusara Siravyadha Sthana 24 - 59

PART (B) - 1) Venous System 60 - 67

2) Physiology of veins 68 - 76

3) Microcirculation 77 - 83

4) Lymphatic System 84 - 87

5) Local Control of Blood flow 88 - 97

6) Regional Venous Systems 98 - 120

7) Blood Letting 121 - 128

IV. DISCUSSION 129 - 138 V. CONCLUSION 139 VI. SUMMARY 140

VII. REFERENCES I - VII

VIII. BIBLIOGRAPHY VIII - XXII

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LIST OF TABLES

Page No.

Table No. 1 - Showing Doshanusara Sirasakhya 9

Table No. 2 - Showing Shakhagata Siras 9

Table No. 3 - Showing Koshtagata Siras 9

Table No. 4 - Showing Urdhvajatrugata Siras 10

Table No. 5 - Showing Classification of Siras According to Varna 14

Table No. 6 - Showing Analysis of Forces of Arterial End of Capillary 20 – 21

Table No. 7 - Showing Roganusara Siravyadha According to Sushruta

& Vagbhata

24

Table No. 8 - Showing Sites for Siravyadha of different Vyadhana

Sthanas of particular Diseases in Lower Limb

39

Table No. 9 - Showing Sites for Siravyadha of different Vyadhana

Sthanas of particular Diseases in Upper Limb

44

Table No. 10 - Showing Details of Kshipra Marma 46

Table No. 11 - Showing Details of Gulpha Marma 50

Table No. 12 - Showing Details of Indrabasti Marma 59

Table No. 13 - Showing Details of Janu Marma 82

Table No. 14 - Showing Classification of According to Varna 130

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LIST OF FIGURES

Fig. 1 - Overall Anterior View of Principal Veins

Fig. 2 - Comparative Structure of Blood Vessels

Fig. 3 - Embryonic Development of Cardio-vascular System and

Blood Vessels

Fig 4 (a) - Diffusion of Fluid through Capillary Walls and

Interstitial Space

Fig 4 (b) - General Organization of Circulatory System

Fig 4 (c) - Functional Structure of Spleen

Fig 4 (d) - Capillary Walls

Fig 4 (e) - Blood Distribution

Fig 5 (a) - Lymphatic System

Fig 5 (b) - Relationship of Lymphatic Capillaries to Tissue Cells

and Blood Capillaries

Fig 5 (c) - Direction of Flow of Lymph and Blood

Fig 5 (d) - Lymphatic Capillary

Fig 6 (a) - Superficial Veins of Head and Neck

Fig 6 (b) - Veins of Thorax and Abdomen

Fig 7 (a) - Superficial Veins of Lowerlimb

Fig.7 (b) - Long Saphenous Vein

Fig 7 (c) - Superficial Veins of Hands

Fig 7 (d) - Superficial Veins of Upper Limb

Fig 7 (e) - Deep Veins of Upper Limb

Fig 8 - Sites for Siravyadha in Different Diseases in Lower

Limb

Fig 9 - Sites for Siravyadha in Different Diseases in Upper

Limb

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Introduction

1

INTRODUCTION

Ayurveda is not only science of medicine but also the way of life style. It is

well organized system of medicine that has unique techniques for harmonious living.

It is not a stagnant one. It was developing through out its history. The science of

Ayurveda has glorious past with extra-ordinarily enriched documentation of medial

literature. That is nothing but experience and observations of ancients.

As Purusha is the conglomeration of soul, mind and body. These three hold

the life processes by maintaining structural and functional dynamism parallelly. In

real sense, Rachana Shareera is the media either to plan for treatment or to achieve the

ultimate aim of life. Hence the fundamental concept of Rachana Shareera has become

basic necessity for both physician and surgeons. That too specially in pre-clinical

studies.

Knowledge of Rachana Shareera is compulsory to students in pre-clinical

studies. Many of the terms appear to be vague for students and teachers leading to lot

of confusions. Because the concepts of Ayurveda Rachana Shareera were evolved

3000 years ago. Now we are lacking the opportunity to clarify the doubts because of

generation gap. Likewise many other concepts appear to be not properly passed onto

the future generation. No doubt Ayurveda is eternal but in present scientific

advancement, we adopt scientific way to popularize the text of Shareera Sthana, in

‘Brihatrayee’ and ‘Laghutrayee’ enlighten the anatomical perspectives in great way.

Still then we are on cross road in accepting the concepts as it is or not. The

two authorities of Ayurveda ‘Charaka’ and ‘Sushruta’ wrote their treatises based on

medicine and surgery. The Rachana Shareera given in Sushruta Samhita Shareera

Sthana is surgical anatomy and that of Charaka Samhita Shareera Sthana is more

metaphysical. Sushruta used the terms with their technical meaning and Charaka used

the terms with their literary usage.

An ancient work in the field of Rachana Shareera by Sushruta, Charaka are

scientific studies. Charaka contributed medicinal anatomy, where Sushruta

contributed surgical anatomy. When, ‘Sira Shareera’, ‘Siravyadha Vidhi Shareera’ of

Sushruta Shareera Sthana are reviewed. Siravyadha is chief line of treatment in

management of many diseases. But here the study is limited to only ‘Urdhwa’ and

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Introduction

2

‘Adha’ Shakhas. Because Sushruta has quoted different Siravyadhana Sthanas in

different diseases. Then a question arises why Sushruta particularly mentioned that

particular Sthana in particular diseases? At this juncture, it has been thought that an

attempt should be made to locate Siras of Siravyadhana Sthanas on the basis of

anatomical, physiological and patho-physiological grounds. Because without proper

interpretation any concept cannot be discarded or accepted.

In present literature, there is gap of knowledge incomplete information

pertaining to Roganusara Siravyadha. To fulfill this gap present study in taken up to

substantiate exact anatomical location of Vedhya Siras in Vyadhana Sthanas of

Urdhwa and Adhah Shakhas in particular diseases conditions with special reference to

phlebotomy in venous system.

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Objectives

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OBJECTIVES OF THE STUDY

1. To provide comprehensive literary information about the concepts of “Sira

Shareera” and “Siravyadha Vidhi Shareera” in general.

2. Co-relative study on anatomical location of Urdhva-Adhah Shakhagata

Vedhya Siras pertaining to particular disease excluding pathological

consideration of diseases.

3. To introspect significance and clinical applicability of Vedhya Siras in clinical

practice based on the knowledge of modern anatomy.

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Etymology of Sira

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1. ETYMOLOGY OF SIRA

Sira Nirukti :

Grammatically Sira Shabda is made up of SZ + k + Tip` = (sri which means Raktavahini Nadi.1

According to Shabdartha Kausthubha, Sira means £ÀgÀ, ±ÀjÃgÀzÀ°ègÀĪÀ £Ár, zÉúÀzÉƼÀV£À £Ár2

Sira Paribhasha :

1. The blood vessels which possess Sarana Karma are called as Siras.1, 3

2. As per the Vedas, the Sira is defined as Hira channel that carries the impure

blood and Dhamani carries pure blood.2, 4.

3. The blood vessels which possess Sarana Karma and circulating throughout

body.5

4. By means of Sarana Karma blood vessels carrying Rasadis from one place to

another place.6

Blood vessels possessing Sarana Karma in Mrudugati are called as

Siras.7 Usually Sira is accepted as vein; in this present day era by transmitter

category of authors even though the term Sira is denoting different meanings

like artery, vessel and nerve. Concerned to this verdict few references we can

quote such as -

1 As per Sushruta and Vagbhata, depending on the nature Sira can be classified

as Sheeta, Shweta, Manda, Kapha.3, 8

2. In Karna 10 types of Siras are present. Three of which should be prevented

from injury.4, 9

3. As the branches of Padminikanda are spreading in Jala, likewise the Siras

from Nabhi are spreading in body in all directions.5, 10

4. Prakupita Vata getting Ashraya in Amsa Sandhi and causing Shoshana of

Sandhi Bandhana resulting into Amsa-shosha that existing Vata causes

Sankocha of Sthanika Siras giving rise to Avabahuka, that means Sira is

considered as ‘Kandara’ [Ligament]. 6,11

5. The circulating blood in Siras causes Dhatu Poorana, Kanti, etc. So may be

considered as Dhamani.7, 12

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Sira Shareera

5

2. SIRA SHAREERA

Sira Utpatti :

1. Nabhi is the place of origin for the Siras and from these they are distributed in

all directions. All the Siras of the body are connected to Nabhi, and are

distributed as a network through out the body. The Pranas are located at the

site of Nabhi and are associated with it. The Siras are radiating from the Nabhi

like spokes from the centre of a wheel. 8, 13 2. Mula Siras (Root veins) are ten, located in the Hridaya, they transport the Rasa

and Ojas to the whole of body. On them, all the activities of the body depend.

They are large at their roots and very small at their tips and appear like the

lines of a leaf. Thus divided and become seven hundred in number.

[Nabhi has been said to be the origin point of Siras. In fetus it can be seen also

that number of veins are attached to Nabhi. After birth all the Siras attached to

Nabhi don’t function9, 14

3. Siras are important in Sandhis as well they transport the Dosha and Dhatus.

All these are attached to the Nabhi further they ramify to approach various

structures of the body.10, 15

Sira Swaroopa :

1. Vatavaha Siras are light red in colour, carrying Vata; Pittavaha Siras are warm

and blue in colour; Kaphavaha Siras are white and stable. Raktavaha Siras are

red in colour neither very hot nor very cold moderately warm.11, 16 [Note : The above statement is not pragmatic normally during health all the

veins appear blue in colour. Throughout the body since non-oxygenated blood

which is blue in colour is flowing through them. Veins might assume other

colours slightly when the blood vitiated by the Doshas are flowing in them. It

is very difficult to distinguish other colours unless observed closely by

experience.]

2. There are 700 Siras. As a garden or grain field is made wet by the water

carrying big and small channels, similarly the Siras by their contractility and

dilatory properly, supply nutrition to the body. They spread all over the body

just like small and minute laminas arising from the central core of the leaf.

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Sira Shareera

6

They originate from the Nabhi and thereby spread all over the body upwards,

downwards and obliquely.12, 17

[Comments : Modern anatomists have never tried to count the exact number

of veins in human body, whereas Sushruta has given the precise number.

Sushruta includes given the precise number. Sushruta includes arteries and

veins both under one heading ‘Sira’. He has also accepted the theory of

‘Kedara-Kulya Nyaya’ postulated in Ayurveda, in reference to body nutrition.]

3. The veins which are bluish-red in colour, small, full and sometime empty

momentarily and having throbbing (pulsation) are carrying blood mixed with

Vata, those which are warm to touch, of quick moment, bluish-yellow in

colour are carrying blood mixed with Pitta; mixture of these signs indicate

mixture of Doshas. Those which are deep seated, evenly placed, smooth and

of slight red colour are carrying pure blood. 13, 18

4. These are two examples of Prananti and Kulya which are corresponding to the

Sthoola and Sukshma Siras respectively. 14,19

Sira Karya:

I. Vata, circulating in their Siras performs physical functions without any

obstruction, promotes the intellect to work proper and prevents the mental

deviations. 15, 20

[Comments : ‘Acharya Dalhana’ has explained the term ‘Kriyanam’ in the

following way – Ik|yiNi> kiyIk|yiNi> p|sirNik&öcni(dni> vik`

Ik|yiNi> BiIPti(dnim` .. This includes both voluntary action and

involuntary action. The word ‘Buddhi Karma’ is related with the five sense

organs and Manas. The intellect plays its role for taking decision in the normal

state. When there is hindrance in the normal functioning of these sense organs.

It is supposed that there is something wrong with the Buddhi or it has gone

under Moha. The Vatavaha Siras perform other actions along with functions

already described.]

A. Vatavaha Sirakarya :

1. ak&(pt vit (sri kiy< :

Vata, circulating in their Siras performs physical functions without any

obstruction, promotes the intellect to work proper and prevents the mental

deviations.16, 21

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Sira Shareera

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2. k&(pt vit (sri kiy< :

When aggravated Vayu occupies its own Siras, it causes various disorders of

Vata.17, 22

B. Pittavaha Sirakarya :

1. ak&Ipt Ip_i Isri kiy< :

Pitta, circulating in its own Siras, gives glow to the body, taste of food,

maintains the digestive power and increases the immunity against diseases. 18,

23

2. k&Ipt Ip_i Isri kiy< :

Pitta when aggravated, moves in its own Siras, produces various disorders of

Pitta. 19, 24

C. Kaphavaha Sirakarya :

1. ak&Ipt kfvhi Isri kiy< :

Kapha, circulating in its own Siras maintains the viscosity of various parts of

the body, stability to the joints, increases the strength and immunity and

performs its other normal functions. 20, 25

2. k&(pt kfvh (sri kiy< : .

When aggravated Kapha occupies its own Siras, various diseases caused by

Kapha appears. 21, 26

D. Raktavaha Sirakarya :

1. ak&Ipt r±tvh Isri kiy< : .

Rakta circulating in its own Siras, nourishes all Dhatus gives colour to the

body, receives tactile sensations and performs its other normal functions. 22, 27

2. k&Ipt r±tvh Isri kiy< : .

When aggravated blood circulates in its own Siras, various disorders of blood

occurs. 23, 28

Sira Sarvavahatvam :

Even though Vata, Pitta, Kapha and Rakta vaha Siras are described. It is also

further classified that there are no exclusive Vatavaha or Pittavaha or Kaphavaha or

Raktavaha Siras; where as all the Siras carry all of them. In abnormal conditions like

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Sira Shareera

8

aggravation of vitiation and vitiation of Dosha, they may circulate in different

direction and different channel. 24, 29

Sira Sankhya :

Doshanusara :

Out of seven hundred Siras, there are forty principal Siras. Out of these 10

carry Vata, 10 carry Pitta, 10 carry Kapha and 10 carry Rakta. The Vata carrying

Siras, situated in the specific receptacle of that principal Vata, branch out in one

hundred and seventy five smaller branches (ramifications). Similarly Pitta carrying

Siras at the site of Pitta, Kapha carrying at the site of Kapha and the blood carrying at

the site of Yakrita and Pleeha are found branching in the same number. In this way

there are seven hundred Siras. 25,30

(I) Vatavaha Siras - 010

Pittavaha Siras - 010

Kaphavaha Siras - 010

Raktavaha Siras - 010

Moola Siras (Total) - 040

(II) Vatasthanagata Siras - 175

Pittasthanagata Siras - 175

Kaphasthanagata Siras - 175

Raktasthanagata Siras - 175

Total - 700

While commenting on this text, Ghanekar has said that the above description

regarding the classification of Siras on the basis of Doshas doesn’t maen that the

forty Siras orginate from Nabhi or Hridaya. By this Sushruta meant that Vatavaha

Siras are thos e which are found in Vata predominating areas, such as Pakvashaya,

Kati, Shroni, Sakti, Asthi, Sparshanendriya (skin). Similarly, Pittavaha and

Kaphavaha Siras are found in Pitta and Kapha predominating areas respectively. To

some extent the above comment seems to be correct, but Sushrutas’ description

regarding classification doesn’t tally with the description given in modern books.

Mula Siras :

Ten Mulasira which are connected to the heart, transport Ojas to all the major

and minor parts of the body. All the activities of the body are dependent on them.

They , dividing themselves to the size of two Angula, one Angula, half Angula, Yava,

half Yava and so on, just like ribs and veins of a leaf become seven hundred. 26,31

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Sira Shareera

9

Vagbhatanusara :

TABLE NO. 1 SHOWING DOSHANUSARA SIRA SANKHYA

(I) Raktayukta Vayuvaha Siras - 175

Raktayukta Pittavaha Siras - 175

Raktayukta Kaphavaha Siras - 175

Raktayukta Shuddha Raktavaha Siras - 175

Total - 700 All Doshas with their normal state, they nourish the body, while on

other hand, if they vitiated cause trouble to the body. 27, 32

Anganusara : 28, 33

(I) Shakhagata Siras :

TABLE NO. 2 SHOWING SHAKHAGATA SIRAS

Vatavaha Siras - 25X4 = 100

Pittavaha Siras - 25X4 = 100

Kaphavaha Siras - 25X4 = 100

Raktavaha Siras - 25X4 = 100

Total = 400

(II) Koshtagata Siras :

TABLE NO. 3 SHOWING KOSHTAGATA SIRAS

Vatavaha Siras - 34

Pittavaha Siras - 34

Kaphavaha Siras - 34

Raktavaha Siras - 34

Total = 136

Guda, Shishna, Shroni - 08

Parshwa - 04

Prushta - 6

Udara - 6

Vankshna - 10

Total = 34

Page 24: Sandhigata siravyadha sr

Sira Shareera

10

(III) Urdhvajatrugata Siras :

TABLE NO. 4 SHOWING URDHVA JATRUGATA SIRAS

(I) Koshtagata Siras Vatavaha Siras - 41 Pittavaha Siras - 41 Kaphavaha Siras - 41 Raktavaha Siras - 41 Total = 164(II) Karnagata - 04 (III) Jihwagata - 06 (IV) Netragata - 08 (V) Greeva - 14 Total = 41

According to Vagbhata,

Guda and Medhragata Siras – 32, Parshwagata Siras – 16, Prustagata Siras –

24, Udaragata Siras – 24, Chest – 40, Greevagata – 24, Hanugata – 16, Jihwagata–16.

Nasagata– 24, Netragata – 65, Karnagata – 16, Shiragata – 20. 34

Out of 700 Siras, four hundred are in the extremities, of which sixteen are not

to be cut, one hundred and thirty six are in the trunk, of which thirty two are not to be

cut, one hundred and sixty-four are at the top, of which fifty are not to be cut. 29, 35

According to Bhela,

It is from the heart that Rasa issues forth and from this (step onwards), the

latter goes to all the places. Heart is reached by the veins and therefore the veins are

said to be born of heart. [This is a clear conception of the heart-artery, vein-heart

cycle of circulation of blood in the body with heart as its centre]. 30, 36 Ten

Dhamanis are attached to the heart. These after going just four inches becomes

twenty (i.e. every one bifurcates). In this way these ten Dhamanis become sixty (i.e.

every one of these bifurcates once again). There in, these sixty Dhamanis become

three hundred thousand networks of Siras. [Such a counting seems to imply a mere

presumptive surmise and not an actual counting out. It is only at the first level that of

the ten arteries from the heart direct observation must have taken place; for many

Page 25: Sandhigata siravyadha sr

Sira Shareera

11

authors agree to this number. To presume that the infinite number of arteries of the

body in hundreds of thousands develops by repetitive forkings from these few initials

of ten is too simplistic]. This is as follows – a tree surrounded by branches comes

down every where by the fruits and the large foliage (Palashas) or as when it gets

stretched or extended down if struck by stones, in a similar way this tree of ramifying

vessels gets extended by the (networks of) Siras (in the body of the person as these

spread out every where). In each and every pit of the hair, there is the exit aperture of

the Sira, from end of which trickles down the sweat. 31, 32, 37

Avedhya Siras :

Those veins which the physician should not puncture, deformity and death are

sure if these are punctured.

The wise physician should know that four hundred veins are present in the

Shakas, 136 in Koshta and 164 in Urdhvajatrugata. Among these 16 in extremities.

Koshtagata-32, Urdhvagata – 50, are to be considered as not suitable for puncturing.

33, 38

Shakhagata Avedhya Siras :

There are hundred Siras in one Sakti, among these one Sira is Jaladhara and 3

internal Siras known as 2 Urvis and one Lohitaksha. They are not fit for venesections.

This description is applicable to the opposite Sakti, in this way Siras in Shakhas are

sixteen. 34, 39

[Comments : Dr Bhaskar Govin Ghanekar has accepted great saphenous vein in

lower extremities and cephalic vein in upper extremity as Jaladhar. Femoral vein in

lower extremity have been considered as Urvi and Lohitaksha Sira. So for as cephalic

and basilar vein are concerned they are superficial structure; therefore, they are to be

protected. Femoral and brachial vein are deep seated structures and should not be

taken for venesection. Venesection is to be performed only where there are minute

veins present. Therefore, Sushruta’s version of contraindicated Siras is practicable.]

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Critics of the term Sira-dhamani

12

3. CRITICS OF THE TERM SIRA-DHAMANI

Critics: 40

After the above collection from classics for an instance, it is necessary to

analyze the word Sira and Dhamani. As per the ancient classics and texts of present

day authors. (Atharva Veda 1/17/1)

As per this context the terms “Sira and Dhamani” are as old as Vedas. They

have been used loosely in common so that there is no specific meanings.

ni(D t& Fm(n: Isri .. (Amarakosha)

This statement stands on wrong basis unfortunately many commentators

followed it. At this junction, such confusions should however be avoided by better

information from Sanskrit scholars. Of course, in explaining certain words, no

specific meanings is denoted still then, Ayurvedists accept that Dhamani and Sira are

not synonymous.

It is important to note that the traditional meanings of Dhamani as artery and

Sira as vein were grasped by ancient lexicographers in Bengal and Maharastra. In

Bengal the anatomists of 19th century, a work “Maha Shareera Tattva” [over 60 years

old of unknown author] and other scholars described arteries as Dhamani and veins as

Siras in their Bengali work in anatomy. In old Bengali dictionary also [“Ashubodha

Abhidhan” over 30 years old] the same meanings have been give to the same words.

In Maharastra traditional knowledge can be found in Prof. V. S. Apte’s Sanskrit

dictionary, Madhava Chandeobha’s Marathi dictionary, V.G. Apte’s Shabda Ratnakar

– in all these works the word “Dhamani” has been interpreted as a ‘blow pipe’, pipe,

an artery [Sudha Raktavahini]. According to Yaksha, the ancient writer of Nirukti

[Vedic lexicon] the word Dhamani has been taken as synonym of speech. In

explaining the Vedic passages quoted by him. Dhamani has been interpreted as pipe

in which there is flow of fluids. Macdonall and Keith in their Vedic index understand

the word Dhamani as pipe. In Rigveda, the term Dhamani commonly implies a pipe

through, there is a flow of fluids. Both the terms Sira and Dhamani frequently seen in

Atharvan Veda. (Atharva Veda – 1/17/3, Atharva Veda – 7/35/2)

According to both stanzas the terms have been used clearly in differently

senses has both of them occur in the same passages. Ex: 100 Hiras (Siras), 1000

Dhamanis.

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Critics of the term Sira-dhamani

13

The interpretations of above stanzas are elaborated clearly by Sayan.

yi[I±t: (A#iy: sÀbIFºy: am*: Eti: p&Ati[ dZÅymini: si[(hnviss:

si[(ht±t vA#i: edZSi[ yi (hri: (sri: rji[vhiniD`y: yIºtgµC(t eRyi(d .

(Sayan Bhashyam)

1. Dhamanis are channels connected to the heart.

2. Thick blood vessels are called as Dhamanis and thin are called as Siras.

3. It is a pity that more than this information is not available in Ayurvedic text.

Although the two terms are used by Charaka and Sushruta, Charaka says that

these are separate channels for the different substances for the system and the heart

and its Dhamanis are source of flow of Rasa. Sushruta speaks more clearly that Sira-

Dhamanis and Srotas all are the same and he established different on another. Because

of (1) distinct characteristic (2) different sources of origin (3) different functions (4)

their usage in Ayurvedic literature in different senses. He then adds usually they

appear similar owing to the close vicinity and similarity of function. The only

question to determined is what is ‘Sira’. Therefore, Charaka’s dictum “¹minit`

Fmºy: srNit` (sri: s|vNit` s|i[ti>(s ..” (Cha. Su.31/1).

It is more illuminating, it starts from root meanings of the terms. According to

Charaka, “¹mi” means to blow and commentators quote blowing or pumping of Rasa

by heart into Dhamanis.

The word “Srotas” is derived from “At\”means slow discharge of fluid. Ex:

capillaries, lymphatics. The word Sira is derived from “sZ” which means move

slowly therefore Sira means channels in which there slow movement. From these

point of view Dhamanis are arteries, Siras are veins and Srotases are lymphatics. In

many passages, Charaka and Sushruta unanimously quote about plenty of portions.

Sushruta uses the term Sira in various places to imply veins in whole of chapter on

“Sira Vyadhavidhi Adhyaya”. On the basis of this it denotes that the Sira is vein.

Judging thus from majority of instances occurring in various places of Charaka and

Sushruta the traditional meaning of Dhamanis appears to be channels from heart. And

of the term “Sira” may be veins. At the same time the term Dhamani has been imply

nerves in many passages of Sushruta Shareera Sthana 9th chapter.

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Critics of the term Sira-dhamani

14

Generally speaking however it is thought Dhamani as artery, Sira as vein

commonly. So it is clear for learned people should over look deliberately to give a

clear statement.

Siravarna Vibhakti :

TABLE NO. 5 SHOWING CLASSIFICATION OF SIRAS ACCORDING TO VARNA

Siraprakara Sirakarya Tridosha Drushtya Vargikaraa

1 Rohinyaha Nourishing body by Upasnehana &

Anugrahana

Artery –

Pittavahi

2 Neela Nourishing body by Upasnehana &

Anugrahana

Veins –

Pittavahinya

3 Gourya Nourishing body by Upasnehana &

Anugrahana

Lymphatics –

Kaphavahinya

4 Aruna Akunchana Prasaranadi Karmas Autonomic Nerves –

Vatavahinya

Transmitter category of author Pandit Gangadhar Shastri shows classification

of Siras. For an instance, he makes the blood vessels identical with Pittavaha Sias and

divides them into two classes, which he calls by two specific terms “Rohini” and

“Neela”. He also includes lymphatics and autonomic nerves in the same table given

above. The Pittavaha Siras have been clearly shown as Raktavahinis. Sushruta divides

the Siras as Vatavahi, Pittavahi, Kaphavahi and Raktavahi.

Page 29: Sandhigata siravyadha sr

Raktamokshana vidhi

15

4. RAKTAMOKSHANA VIDHI

Introduction :

Raktamokshana is being one of the Shodhana therapy as per Sushruta and

Vagbhata. Raktamokshana is nothing but letting of blood outside the body, where

alone is equal to all measures described in the treatment of diseases caused by

Raktadusti. Rakta is said to be the base for origin of the body. It is the backbone of

life. Pure blood is the back of the health, colour, pleasure and life span. 35, 41

Shareerasta Ahara Prasada Rasa is getting modification by Ranjaka Pitta

called Rakta. In brief regarding its significance is concerned. 42 Rakta is being

Pradhana Poshaka of body where Shareera existing by Rakta itself. So it is essential to

preserve Rakta. 36, 43

By the above quotations Rakta is very significant in maintaining physiological

well-being, where it’s vitiation causes serious illness. So in many places Sushruta

considers Rakta as also one of the Dosha. Likewise Vagbhata has also given same

preference to Rakta as Sushruta. So also Raktamokshana is considered as one of

Shodhana therapy according to Sushruta and Vagbhata.

Raktamokshana is two types 37, 44

(1) Shastravacharana

(2) Anushastravacharana

Any of the above modalities are adopted according to Dosha, Rakta and Atura

Avasthas.

In Vatadushti Shringavacharana is as Shringa of cow is Ushna, Madhura,

Snigdha which opponents of Sheeta, Rooksha. In Pittadushti Jaloukas are selected as

they are being in Jala. They are Sheeta and Madhura, opponents of Pitta. In

Kaphadusti Alabu is selected as it is having Katu Rasa, Rooksha, Teekshna Gunas.46

According to Rakta-Avastha, So that if it is Avaghada [superficial] then

Pracchanna, Jalouka, Alabu, Shringa etc. can be adopted. If there is Sarvadaihika

Raktadusti Siravyadha can be adopted. 47

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Raktamokshana vidhi

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Depending on Atura Bala also different modalities of Raktamokshana are

selected. So that in Raja, Bala, Vrudha, Sukumara, Nari Anushastravacharana can be

adopted in others. Shastravacharana can be adopted. 48

Out of all types of Raktamokshana as Siravyadha is taken up for study it is

highlighted in detail.

r±tmi[xN 38, 45

SAt\(vs\ivn an&SAt\(vs\ivn

SZ>g p\Cºn (sriÄyF jli]k

lib&

Page 31: Sandhigata siravyadha sr

Siravyadha vidhi

17

5. SIRAVYADHA VIDHI

Siravyadha is done to let out the blood without producing any untoward

effects on the individual. The selection of the disease and site of the texts. As the Siras

are ot being in fixed place it needs skilled hand. In addiction to instruments, drugs and

other items should be kept handy. The selection of Yantra-Shastras can be made as

per wisdom of the surgeon according to site, disease and availability of instruments.

Therefore adoption of the development of science and technology on par with proper

utilitzation of advanced instruments is permitted and also necessary for the

implementation of theory and to prevent the complications. 54

Historical Background of Siravyadha :

1. Siravyadha is being one of the effective methods explained by Sushruta for the

letting of blood outside the body.49

2. In Shodhana therapy Raktamokshana has been explained as one of the type of

Panchakarma procedure, under which Siravyadha i.e. also considered as an

effective parasurgical procedure. 50

3. It was also practiced in Vedic period to alleviate the swelling. In Kaushika

Sutra of Atharvana Veda have references regarding Raktamokshana by

Shringana is case of Pravavata has been done under the guidance of Buddha.51

4. It is one of the Shalyatantra technique adopted by most of ancient Ayurvedic

scholars and practiced through ages such as [Vaidya Shatapatha Brahmana,

Oupadenava, Ourabhra, Poushkalavata, Karaveerya, Vaitaran, Bhoja,

Kritavirya, Gopura Rakshita, Bhaluki, Kapila, Goutami etc.]. Moreover

Charaka, Sushruta, Vagabhata and others have explained regarding

Raktamokshana. In period of 1200-600 A D extensive practice of parasurgical

procedures were practiced by Unani practioners and during 1300 A D in

Europe. There is evidence of Raktamokshana are available. During 1200 A. D.

Hakeems and Unani practioners were extensively practicing blood letting in

many skin diseases.King Jahangir was also having the habit of blood letting

once in an year. 52

5. During 18th century blood letting was done to whom it was understood that all

other side said treatments were help less and the blood letting was followed to

Page 32: Sandhigata siravyadha sr

Siravyadha vidhi

18

maintain physiological well-being. Auto-haemotherapy is extremely used in

dermatology as it has a marked hyposensitizing effect and promotes the

immunologic reactivity. The blood taken from ulnar vein of the affected

person is injected into gluteal muscles E levi has treated many cases of

typhoid in adults of auto-haemotherapy in which 5-10 cc of blood was

removed from veins of arm and re-injected to subcutaneously at once into

lumbo-sacral region. The injections was being repeated twice or thrice on

every five days. The procedure is quite harmless and resulted in rapid fall in

temperature with improvement of general condition. 53

Poorvakarma :

1. Siravyadha Yogya – Ayogya Atura Vichara

2. Upakarana Siddhata

3. Atura Siddhata

1. Siravyadha Yogya-Ayogya Vichara :

a. Siravyadha Yogya: 39, 55

a. All Raktapradoshaja Vikaras h. Mukharoga

b. Especially Vagbhatokta Vikaras

such as Visarpa

i.

Netraroga

c. Vidhradhi j. Mada

d. Pleeha Vruddhi k. Trushna

e. Gulma l. Kushta

f. Agnimandya m. Raktapitta

g. Jwara n. Shrama

b. Siravyadha Ayogya Purusha: 40

a. Bala j. Garbhini

b. Vruddha k. Kasa

c. Ruksha Shareerayukta l. Shwasa

d. Ksheena m. Shosha

e. Parishramita n. Jwara

f. Madyapeeta o. Akshepa

g. Krusha p. Pakshagata

h. Panchakarma Neyojita q. Moorcha etc.

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Siravyadha vidhi

19

i. Klaibya r.

Siravyadha Kala :

In Shubhadivas, when the environment is not too cold and not too hot41

,

especially Sheetakala is recommended for Siravyadha so that in Varsharutu when

there are no clouds, in Greeshmarutu when there is cold environment. In Hemanthrutu

Madhyahna Kala are recommended as Siravyadha Kalas.42, 56

(2) Upakarana Siddhata: 57

According to the situation of Siras, different instruments are used for

Siravydha.

(i). Kutarika : If Sira is just over bones this can be used. This is flat, and like

tooth of cow and edge is ½ Angula. It is hold in middle finger and thumb of

sight hand and by left hand Sira is to be fixed and cut.

(ii). Vrihimukha Shastra : If Siras are in Mamsala Sthana this Vrihimukha

Shastra is used for Siravyadha. It is useful in Udaragata Siravyadha. Its handle

is ½ Angula and its Vrithagrabhaga is hold between finger and used.

(iii). Trikurchika : This is used in Bala, Vriddha, Sukumara, Sthree. Other

materials like Karpasa, Pattika, Tourniquet, Pichu, artery forceps, scissors,

rubber tube, connection tube, Kachapatra, medicated oil like Jatyadi Taila,

Udumbar Choorna and according to the disease and Sthana of Siravyadha

different Anushastras are kept ready.

3. Atur Siddhata:

The patient is made Yogya to Siravyadha prior to the process. He is given

internally Snehasadhyas, externally Abhyanga and Sarvanga Swedana, after which

patient is fed with curd mixed diet, Yavagu, Jangala Mamsa Rasa to cause Utklesha in

Raktadhatu so that it comes out devoid of any hindrance. And in suitable position

according to Sthana of Siravyadha making Sira to become prominent by tourniquet.

43, 58

Pradhana Karma :

1. Siravyadhanarth Asana (Position of patients during Siravedha)

2. Roganusara Vedhya Sira Vichara

3. Observation during Siravydha

4. Observation of Dustaviddha Siras

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Siravyadha vidhi

20

1. Siravyadhanartha Asana: 59

(i). Shiragata Siravyadha :

Patient is made to sit on stool facing towards sun knees flexed. And both

elbows should be placed at knee joints and fore hands towards neck. And is

tied. The Sira is made to become dominant. Patient is asked to hold air in

mouth for easy expulsion of blood this is done only in Bahirmukha Siras.

(ii). Padagata Siravyadha:

In Siravydha of legs patient should be in sitting position with one leg stretched

where Siravydha is going to be done and another slightly flexed. Leg is tied to

prevent vibrations and to make the Sira to become dominant at the time of

blood letting Gulfasthana should be gently massaged.

(iii). Hastagata Siravyadha :

Thumb is held inside the wrist and suitable position Hastagata Siravyaha is

done.

(2). Roganusara Siravyadha: 60

TABLE NO. 6 SHOWING SITE OF SIRAVYADHA ACCORDING TO SUSHRUTA AND VAGBHATA

S. N. Disease Sushruta Vedhya Sira Vagbhata Vedhya Sira

1. Padadaha Padaharsha Chippa Vatarakta Vicharchika Padadari Vatakantaka Avabahuka

2 Angula above from Kshipra Marma Except Avabahuka Visarpa, Vicharchika others’ are according to Sushruta

2. Kroshtuka Sheersha, Kanja Pangu

4 Angula above from Gulpha in Jangaha

Except Khanja Pangu others according to Sushruta

3. Grudhrasi 4 Angula above or below from Janu Sandhi

According to Sushruta

4. Moorta Vriddhi Behind Vrishana Sthita Sira - 5. Jalodara 4 Angula behind from Nabhi Vama

Parshwa -

6. Antravidhradhi Parshwashoola

Sira in between Vaksha and Sthana According to Sushruta

7. Bahushosha Avabahuka

Sira in between two Amsas -

8. Truteeyak Jwara Sira in between Trikasandhi According to Sushruta

9. Chaturtaka Jwara

Below Amsa-sandhi According to Sushruta

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Siravyadha vidhi

21

10. Apasmara Below Hanusandhi Hanu or Bhroo Madhya Sira

11. Unmada Between Keshanta and Shankha or Urahapradesha or Lalata or Sira of

Apanga

Vraha Apanga and Lalata

12. Jeehwaroga Danta Roga

Sira below Jeehwa -

13. Mukharoga - Sira being in Jeehwa, Ostha, Hanu and Talu

14. Taluroga Talugata Sira - 15. Karnaroga Sira above Karna Karnaga Sira

Vyadhana 16. Nasaroga Nasagra Sira Acc. to Sushruta 17. Peenasa - In between Nasa and

Lalata 18. Timira

Akshipaka Shiraroga Adhimanta

Upanasika Sira Latata Sira

Apanga Sira

According to Sushruta

19. Jatroordhava Granthi

- Greeva Karna, Shiragata Sira

(3) Siravyadha Nireekshana: 61

As the aim of Siravyadha is to let out vitiated blood, just after Siravyadha

Doshita Rakta is only coming out as yellowish liquid comes out where

Kusumbha Pushpa is punctured.

Samyak Srava Lakshana :

Automatic stoppage of blood after certain time is on indication of “Samyak

Siravyadha” and it also indicates that complete vitiated blood is expelled out. Then

patient feels light, pain subsides, Rogalakshanas are decreased called “Samyak

Vriddha” Lakshanas.

Asamyak Srava Lakshana :

“Asamyak Sravita” Rakta will cause Daha, Raga, Pakadi Laxanas when

Siravyadha is done in hot conditions, Adhika Swedana, Atividdhata will cause

Atisrava Laxanas like Shirobhitapa, Adhimanta, Timira, Dhatukshaya, Akshepaka,

Pakshaghata, Yekangaroga, Hikka, Shwasa, Kasa, Pandu and lastly Marana. When

position of the patient is not proper when Sira is not prominent of Shastra is not sharp.

If Swedana is not given properly, just after meals Mada, Moorcha, Shrama. In these

conditions, even though after Samyak Siravyadha also Samyak Rakta Srava is not

taking place.

(i) Upachara :

Page 36: Sandhigata siravyadha sr

Siravyadha vidhi

22

If there is Aparavrutta Raktasrava any three of, Karpura, Tagara, Devadaru,

Vidanga, Chitraka, Trikatu, Haridra, Karanja, taken and powdered. Mixing it with

Saindhava Lavana and Tila Taila Vrinamukha is gently massaged to provide Samyak

Pravruttata of Rakta. If there is Atirakta Srava, so as to prevent it different measures

can be taken.

1. Lodhra Yasti, Priyangu, Sarjarasa, Gairika, Rasanjana, Shalmali Pushpa

Choorna of these drugs, is applied over Vranamukha of Siravyadha.

2. Arimeda, Medrasingi, Sala, Sarjarasa Twak Choorna is mixed with Madhu

and applied.

3. Sheetal Bhojana, Sheetal Avachoornana.

4. Kshara-Agni Dahana.

(ii). Raktasrava Niyama: 44, 62

In persons who are strong, who have great accumulation of Doshas and who

are of suitable age, experts desire, one Prastha (640 ml) of blood be allowed to flow

out after venous puncture.

At once completely whole vitiated blood should not be letted out, for

remaining Dosha Shamana Chikitsa may be followed according to Rogabala,

Rogibala the fixed quantity of blood is letted. Uttama – 1 Prastha, Madhyama – ½

Prastha, Vagbhata says that 1 Kudava or 3 Pala or 13 Tola may also be letted out to

prevent the complications.

(4). Dusthaviddha Sira Nirikshana: 45, 63

Dusta Vedhya Laxanas are 20. These are Siravyadha Vyapats. (a) Durviddha

(b). Atividdha (c). Kunchita (d). Picchita (e) Kuttita (f) Aprasoota (g) Atyudeerna (i)

Atividdha (j) Parishuska (k) Kunita (l) Vepita (m) Anushita Viddha (n) Shastrahata

(o) Teeryakviddha (p) Apaviddha (q) Ayadha (r) Vidhruta (s) Dhenuka (t) Punah-

Punah Vidha (u) Sirasnayvasthi Viddha.

Paschat Karma: 64

1. Upadrava Chikitsa

2. Pariharya Vishaya

3. Shamanoushadhi Chikitsa

1. Upadrava Chikitsa : During Siravyadha if any Asrava, Alpasrava or Atisrava

they should be treated.

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2. Pariharya Vishaya : Here Agnirakshaka Vishesha Pathya Yojana is followed

such as Natisheetoshna Bhojana, Rakta Vardhaka Annapana should be taken

Vata Prakopaka activities should be promoted.

3. Shamanoushadha Chikitsa : Afte Rakta Mokshana Vishesha Shamanoushadha

Chikitsa is followed .

a. After this – (1) Weekly once for 3-4 times blood letting may be done

(2) If in first sitting not letted then after 15 days once again blood

letting is followed.

Pradhanyata of Siravyadha :

1. As Basti has been mentioned as dominant line of treatment in Kayachikitsa,

likewise Siravyadha has been mentioned as dominant parasurgical procedure

in Shalya Tantra for the letting of blood outside the body. So it is considered

as 50 % of Shalyachikitsa. As Rogadhisthana primarily being Rakta so

Raktamokshana by Siravyadha has got its own importance in curing the

disease. 46, 65

2. Vagbhata also mentioned that Siravyadha is complete treatment in

Shalyatantra as Basti is the complete treatment in Kayachikitsa. As Rakta

Dhatu is the main causative factor in all Vikaras or disease. So it is to be

treated first by Siravyadha Vidhi. 47, 66

3. Raktamokshana by Siravyadha will be helpful to maintain good health by

causing Vrana, Prasannata, Indriya Prasannata, Agnideepti, proper Vega

Pravruthatha, Pusthi, Tushti etc. 48, 67

4. Siravyadha is the supreme procedure amongst all Shodhana therapies. When

Snehadi, Lepanadi treatments have been failed Siravyadha will be followed. 49,

68

5. Diseases of the skin, tumours, oedema and diseases arising from blood will

never occur in persons indulging in blood letting. 50, 69

6. In Rakta Pradoshaja Vikaras Siravyadha is supreme procedure which gives

complete permanent cure rather than other types of Mokshana and other

Shodhana therapies like Vamana-Virechana etc.70

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6. ROGANUSARA SIRAVYADHA STHANA

(I). ADHASHAKHAGATA VEDHYA SIRA STHANAS : [Fig. 8]

In diseases such as Padadaha, Padaharsha (tenderness / tingling in the soles),

Chippa (whitlow), Visarpa (erysipelas), Vatashonita (gout), Vatakantaka (sprain of

the ankle), Vicharchika (a skin disease) and Padadari (fissures of soles) etc., the vein

situated two Angula (4 cm) above the Kshipra Marma should be punctured using

Vrihimukha Shastra. 51, 71

As per the quotation Siravyadha is done in the said diseases 2 Angula above

from Kshipra Marma. The anatomical location of vein that part is interpreted on

available anatomical grounds.

Usually Marma Sthanas are contraindicated for Siravyadha. Regarding

“KSHIPRA” 72 Marma is concerned gives a meaning of quick due to its immediate

effect.

TABLE NO. 7 SHOWING DETAILS OF KSHIPRA MARMA

Measure & Type - 2 in number, Snayu, ½ Anguli

Site - In between the big toe and the first toe. Controls

Rasavaha, Pranavaha, Avalambaka and heart.

Tissues involved

(Anatomical

structures)

- Abductor hallucis brevis, lumbricalis muscles, posterior

tibial nerve, dorsal metatarsal artery, plantar arch and

medial plantar artery, metatarso-phalangeal joint.

Signs if injured - Injury may cause impairment of the function of the

abduction and flexion of the great toe. Damage to the

artery may cause severe bleeding, haematoma, inside the

plantar aponeurosis and septic toxaemia. It is Kalantara

Pranahara type Marma

As the site of Vyadhana is two Angula above from the Kshipra Marma that is

usually the branch of great saphenous vein. Where it is the longest vein in the body,

ascend from foot to the groin in the subcutaneous layer. It begin medial end of the

dorsal venous arches of the foot. The dorsal venous arches are network of veins on the

dorsum of the foot formed by dorsal digital veins draining blood from toes and unite

in pairs to form the dorsal metatarsal veins. As dorsal metatarsal veins approach a foot

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they combines to form dorsal venous arch. 73 So as per the above context in all said

diseases Siravyadha is done in dorsal venous arch. The dorsal venous arch above two

Angula of Kshipra Marma is the choice sites for venu-puncture. 74

PADADAHA :

Vayu combined with Pitta and Rakta causes burning sensation in fact

particularly while walking. It is know as ‘Padadaha’. The pain is pronounced while

walking and it is mild when standing. 52, 75

The condition ‘Padadaha’ can be correlated to in one or other way to the

thiamine, pantathenic acid deficiency called burning feet syndrome. Usually thiamine

aspartes in metabolic systems of the body, principally as thiamine pyrophosphate.

Thiamine deficiency causes decreased utilization of pyruvic acid and some

aminoacids by the tissues. But increases the utilization of fats, producing 3 target

tissues : (a). peripheral nerves (b). heart and (c). brain. Decreased utilization of these

nutrients is the responsible factors for many debilities associated with thiamine

deficiency. Pantothanic acid widely distributed in fruits, therefore, existence of

clinical deficiency in human is doubtful. Claims have been made as “burning feet

syndrome”. It is characterized by pain in the feet, burning in character. The symptoms

are worst on walking and night. Previously it was thought to be beri-beri.76 Thiamine

deficiency can also cause degeneration of myelin sheath of nerve fibres both in

peripheral and central nervous system. It can be treated by riboflavin and calcium

pantothenate.

Critics:

As the condition shows involvement of Rakta and Pitta Doshas in the

causation of disease, Raktamokshana by Siravyadha is recommended in Pada itself.

Two Angula above from Kshipra Marma. In Pada that is the site where we get easily

available superficial vein. As Adhisthana is being Pada in ‘Padadaha’, this is the site

of Siravyadha in Padadaha. When pathophysiology of Padadaha is concerned it is

nothing but “burning feet syndrome of thiamine deficiency”, which leads to

incomplete metabolism of carbohydrate resulting accumulation of pyruvic acid, which

is a reason for burning sensation of feet. One of the most fundamental principles of

circulatory function is the aility of each tissue to control its own blood flow in

proportion to its metabolic needs. As the need for blood flow changes, the blood flow

also changes. Some specific needs of the tissue for blood flow are delivery of o2,

nutrients such as protein, glucose, carbohydrate, amino acids, fatty acids, etc. removal

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of metabolites, transport of hormones. In general, greater the metabolism greater the

blood flow.

So here, by doing blood letting by Siravyadha, in the site which is nothing but

dorsal venous arch, venous pressure can be relieved, fresh blood is rushed towards the

part. So metabolic activity of the part is increased concurrently accumulated excessive

pyruvic acid is drained by which local homeostatis is maintained. So in Padadaha in

the site two Angula above from Kshipra Marma that is dorsal venous arch which is

superficial and easily accessible. On the basis of these backgrounds the site told by

Sushruta and Vagbhata in Padadaha cannot be discarded.77

PADAHARSHA :

Accoring to Sushruta, Padadaha is nothing but the legs have tingling sensation

(feeling of pain and needle) and gradually numbness occurs. This disease is known as

“Padaharsha” and is caused by aggravation of Kapha and Vata together.53, 78

Padaharsha can be correlated to that of “tingling and numbness”. Common

types of parasthesia, commonly seen in neuropathies due to various causes. Presently

the condition is correlated to peripheral neuropathy due to type-II NIDDM. Here

plasma glucose remains normal, insulin levels are elevated. Insulin resistance tends to

worsen despite of elevated insulin concentrations. At last insulin resistance did not

change, but insulin secretion declines resulting into fasting hyperglycemia. Glucose

uptake and glycosis are impaired. So gradually degenerative changes of nerves,

characteristically symmetrical as tingling, pricking, burning and numbness.

Critics :

Because of the aggravation of Vata and Kapha, Padaharsha is manifested so

that peripheral parts of the lower limbs have got tingling and numbness. It has been

pointed out that by means of Sthanika Siravyadha, Doshas are neutralized and

features relieved. So, Siravyadha is done two Angula above from Kshipra Marma, as

Rogadhisthana is Pada and that site often recommended because of superficially

available veins.

When the concept is correlated to modern science, is a type of parasthesia

commonly seen in neuropathy of various causes. Presently the condition is taken up

as neuropathy due to Type-II NIDDM. Here because of insulin resistance of cells,

fasting hyperglycemia is resulted when glucose uptake and glycolysis are impaired

there is gradually generative changes of nerves, characterized by tingling and

numbness. Glycolysis means splitting of pyruvic acid by different chemical reaction.

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This end product is oxidized to release energy. By means of blood letting by

phlebotomy, there is increase in insulin sensitivity in individuals with type-II diabetes.

That results in proper glucose uptake and glycolysis which can prevent degeneration

of nerves by the release of energy.

Overall, by phlebotomy the local cellular metabolism is improved, blood flow

improved, providing required nutrients to the nerves. So in “Padaharsha” or

“neuropathy” , venesection is done in dorsal venous arch. On the basis of this patho-

physiological ground, the site of Siravyadha dealt by Sushruta may be accepted. 79,80

CHIPPA :

Dushita Pitta and Vata is getting Ashraya in “Nakha-Mamsa” resulting into

pain, burning and ripening so called Chippa. 54

Vitiated Vata and Pitta is situating in ‘Nakha-Mamsa’ Pradesha and causes the

Vruna of Nakha Mamsa. It is called as ‘Akshat Roga’. 55, 81

This is correlated with Paronychia This is the most common infectioin of nail

bud of fingers. Sings include redness, tenderness, lymphangitis, lymphadenopathy etc.

After the inflammatory phase, pus is trapped besidest the nail. Sometime it may

become chronic where pus is trapped between fibrous septae, which binds skin to the

underlying bone can get into infection. 82

Critics :

There is involvement of Pitta and Vata getting Ashraya in ‘Nakha-mamsa’

resulting Vruna Shotha Laxanas. Such as pain, burning, ripening. Adhisthana being

‘Nakha’, Siravyadha is done 2 Angula above from ‘Kshipra Marma’, which can help

to resolve Vrunashotha Laxanas. When modern correlation is done, is nothing, but

‘nail bud infection’ of fingers. Blood letting by Siravyadha, venous drainage of part is

increased associated with rush of blood supply where endothelial cells are sensitive to

alteration in blood flow. They undergo certain changes facilitating migration of

lymphocytes through vessel wall subsiding local infection, inflammation, providing

improvement in metabolism of cells.

So here also the same branches of dorsal vein arch is selected for phlebotomy.

VISARPA :

By means of Mithya-ahara-vihara like Adhika Lavana-Amla-Katu-Ushna-

Vidahi and Adhika Madya Sevana, Adhyashana (Divaswapna) Vatadi Doshas get

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increased they will enter in the Twacha, Mamsa and Rakta. Vitiation will not persists

in one place but it is spreading in nature. According to Dosha dominancy Shotha is

seen called ‘Visarpa’. 56, 83

Dosha-Dushya Sambandha: 57, 84

Dosha Vata, Pitta, Kapha.

Dushya Rakta, Lasika , Twacha and Mamsa.

All the Doshas are responsible and Twak, Mamsa, Lasika and Rakta are

involved. According to Sushruta it is of 4 types – Vataja, Pittaja, Kshataja and

Kaphaja and Tridoshaja. But the common features can be Vedana, Jwara. Shotha

depending on Doshik, involvement of the features are different. Individual Doshaja

are Sadhya and Tridoshaja, Kshataja Asadhya. 85

The features of Visarpa are correlated with cellulitis, erysipelas and herpes

zoster.

Erysipelas: 86

It is spreading lymphangitis, where the causative organism is streptococcus

pyogenes. Poor hygienic living, recurrent URI, chronic illness are the predisposing

causes. But the lesions starts as a scratch, it commences as a rose pink rash which

extends to the skin, vesicles appear sooner or later over the rash and rupture. A serous

discharge comes out from these vesicles. To distinguish between erysipelas and

cellulitis is that, erysipelas as a typical rosy-red rash, on pressure it feels stiff, the

vesicles of erysipelas contain serum. The common sites are face, upper and lower

extremities.

It is a form of cellulitis characterized by bright red appearance of involved

skin. The region is warm, tender, swollen, shiny. It is almost always due to beta-

hemolytic streptoccus. They tend to develop lymphangitis where lymphatic drainage

is disrupted, commonly affect in lower extremity.

Herpes zoster:

Varicella zoster is a virus causing herpes zoster. It usually develops in more

than 40 years, approximately 5 % of patients experience recurrence. The condition

begins as an infection accompanied by fever, malaise, and anorexia, maculo-papular

rashes, usually on upper trunk and face. It is recurrent painful, vascular eruption

cuased by reactivation of chickenpox. It is self limited disease in young and healthy

persons, but cool compressors, anti histamines, analgesics are sufficient. On

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reactivation of the virus produced by ganglia to the sensory nerve and peripheral

nerves. Always it presents as a dermatological vascular rash with pain. Trasmission

likely to take place by respiratory route. The subsequent localization leads to seeding

of reticulo-endothelial system, developing viraemia. Results in difused, scattered skin

lesions involving dermis.

Critics:

When we have reviewed the Samprapti of Visarpa, there is involvement of

Vata, Pitta, and Kapha Doshas, Rakta, Lasika, Twacha, Mamsa causing Visarpavat

Shotha. As per the classical references itself; Ekadoshaja Sadhya, Tridoshaja

Kashtasadhya. By Siravyadha two Angulas from Kshipra Marma, Sthanika Shodhana

occurs, where Rakata, Twacha, Mamsna, Lasika-Dusti is neutralized. So Sthanika

Raktamokshana is recommended from the available vein. When features of Visarpa

are seen most probably it is similar to cellulitis, erysipelas and herpes zoster.

The cellulitis spreading inflammation of subcutaneous tissue by causative

organisms like streptococcus or staphylococcus, resulting in swelling, pain, redness

etc.

By means of the blood letting from the site, venous drainage is improved.

Blood is rushed towards the part, WBCs, macrophages were rushed towards the part

to engulf the infectious agents. So immediately inflammatory changes are neutralized.

As local cellular metabolism is improved. So blood letting by phlebotomy told by

Sushruta may be considered.

Another condition can be taken as erysipelas which is nothing but spreading

lymphangitis (inflammation of lymphatic vessels). Lymphatic system is a accessory

route where 1/10th of interstitial fluid is drained. Almost all tissues of the body have

lymphatic channels which drain excessive fluids directly from interstitial spaces.

Lymph returns proteins from tissue spaces. It removes the bacteria, toxins foreign

bodies. So whenever there is any inflammation in lymphatic channels. The excess

protein are left in interstitial space, bacteria, toxins are also not drained. But when

phlebotomy is done, local intravascular pressure is decreased, where in pressure of

interstitial fluid is also decreased. Lymphatic capillary permeability is increased to

improve lymphatic circulation. And also stimulation by endothelial cells, there is a

release of cytokines, scattering of WBC to neutralized infectious agents. In this way

blood letting in dorsal venous arch may be considered.

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As varicella zoster virus is directly affecting reticuloendothelial system and

peripheral nerve routes, definitely local Siravyadha helps. Because by means of local

blood letting, there is a stimulation of reticuloendothelial system to produce

erythropoietin decreasing viraemia. Reactivation of virus is stopped as WBC are

scattering towards the affected part. Nerve inflammation is also decreased by

production of steroid hormones. So blood letting in dorsal venous arch may help in

‘herpes zoster’.

VATARAKTA :

Rakta is severly vitiated by Vata Dosha resulting particular disease condition

called Vatarakta.

Sukumara Prakrutiyukta, Mithya-Ahara-Vihara-Sevita, Shokatapta, Adhika

Stree-Sambhogi, Adhika Vyayama, Madya Sevita, Satmya Vipareeta Ahara-Vihara,

Vishama Prayoga of Sneha, Avyavayita, Sthoolatwa, Ati-Lavana, Amla, Katu,

Kshara, Ushna Padartha Sevana, Ati Sevana of Tila, Moola, Shakha, Masha,

excessive intake of Ikshu, Dadhi, Sura, Asava etc. 58, 87

Samprapti : 59, 88

Vataprakopa immediately leads to vitiation of Rakta Vayu-Margavarodha

again excess Raktadusti by Vata as these Vata dominancy is called Vatarakta.

According to Dosha dominancy features are seen.

Laxanas :

1. Toda

2. Bheda (pricking pain)

3. Cracks

4. Dryness

5. Excess temperature

6. Redness

7. Swelling

Sometimes Sarvadaihika Laxanas can also be seen so that pain in Angustha,

Gulfa Sandhi, Janusandhi, Manibandha Sandhi etc.

The condition may be correlated to metabolic disorders. Where purine

metabolism is impaired and serum uric acid level is high, may be because of

excessive production or inadequate excretion i.e. hyperurecaemia. The pathogenesis is

unclear, certain factors have been implicated to cause this condition such as gout, RA,

OA, achronosis, hyperparathyroidism. The involvement may be non-articular or poly-

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articular, but often big joints are affected. Urate crystals are actually irritating and

result in acute pain. The skin is overlapping red, warm oedematous. Crystals of

sodium biureate may be deposited in bone, in cartilage and joints.

Clinical Features :

1. It has abrupt onset particularly pain, swelling, tenderness, temperature of first

meta-tarsal joints

2. Frequent attacks disrupt sleep,

3. Sometimes inflammation is of gross that it may resemble cellulitis.

4. Mild attacks resolve spontaneously within two days. Severe attacks may last

for seven to ten days.

Critics :

In Vatarakta, there is immediate vitiation of Rakta resulting Vayu

Margavarodha again excess Raktadusti called Vatarakta, characterized by Thoda,

Bheda, Raktima and Shotha of Hastha, Pada and Sandhi, especially knee joint. By

Raktamokshana at 2 Angula above from Kshipra Marma will definitely help. Here

Dooshita Rakta is expelled out relieving Vayu Margarodha, where vitiated Vata

becomes neutral resulting into relief from the symptoms.

The condition may be correlated by metabolic disorder, where purine

metabolism is impaired and serum uric acid is high may be because of excessive

production or inadequate excretion, that is ‘hyperuricaemia’. In general an

homeostatic mechanisms are concerned there must be removal of metabolic end

products like carbon dioxide which is abundant of all end product of metabolism.

Passage of blood through the kidneys removes most of other substances

besides co2 from plasma, which are not needed by the cells. The substances include

different end product of cellular metabolism, such as urea and uric acid. If they are in

excess they might have accumulated in extracellular fluid. The kidneys perform their

function by filtering large quantity of plasma and reabsorbing substance needed by the

body like glucose, aminoacids, water etc. Most substances are not need by the body

especially metabolic endproducts urea, uric acid are poorly reabsorbed, instead pass

on through the renal tubules into the urine.

In general local blood letting is done by venesection, certain amount of urea,

uric acid might have taken away and there is a release of ‘angitensin’ hormone,

which has got renal and adreno-cortical stimulatory effect providing excretion of

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urea, uric acid by the kidneys. That is why in gouty arthritis, blood letting is done in

branch of dorsal venous arch. 89

VATAKANTAKA :

Walk on the hard roads, surface causes Vata Prakopa and produces pain in the

‘Pada’ called ‘Vatakantaka’. 60, 90

Walking on undue surface, exercise leads to vitiation of Vata in the ankle

joints produces pain in the heel that condition is called as Vatakantaka.91

The condition can be correlated to ‘Heel spurs’ or calcaneum spur. ‘Spur’

means bony growth. Heel spur often occurs in heels i.e. calcaneum bone.

Predisposing Factors :

1. Obesity (Excess weight on heel of feet)

2. Ill fitting shoes wearing for longer duration

3. Pronation – means abnormal movements of the foot.

Pathology :

Bony outgrowth usually extend from the heel bone into the soft tissue

surrounding the bottom of the foot causing inflammation of plantar fascia (fascitis)

and pain through out the heel of the foot. That heel spur is composed of calcium

deposits. This bony deposits develop when the plantar fascia stretches abnormally due

to stress factors and occurs where the ligament attaches and stretches away from the

heel bone. 92

Features:

1. Serious pain in the heel of the foot.

2. Generate aching pain with every step.

3. Sharp – pricking type of pain in heel.

4. More in morning hours. Critics :

According to Ayurveda, because of Vata Prakopa, pain resulting into Pada

especially in Gulfa Sandhi (heel of foot) called Vatakantaka. By means of Sthanika

Raktamokshana by Siravyadha, Vata gets neutralized and pain relieved. So blood

letting is done two Angula above from ‘Kshipra Marma’. When the condition is

correlated, it is nothing but “heel spur”. Especially, calcaneum bone is affected, so

called ‘calcaneum spur’. It is nothing but bony out growth, composed by calcium

deposit, pressing over the plantar fascia.

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When normal mechanism of bone calcification is concerned, it is nothing but

secretion of collagen molecules and ground substances, by osteoblast. These

osteoblast become entrapped called osteocytes. The osteoblasts also secrete a

substance into osteocytes, to neutralize an inhibitor called pyrophosphate. So under

normal conditions, there is limited growth of bone. In abnormal conditions, calcium

salts precipitate in arterial walls called arteriosclerosis. Likewise, calcium salts

frequently deposit in degenerative tissues. The osteoblasts secret large quantity

alkaline phosphatase, when they are actively deposited on bone matrix. This

phosphate is believed either to increase local concentration inorganic phosphate are

active collagen fibres. In such a way they cause deposition of calcium salts. As

alkaline phosphate is defuses in blood its level is indicator of rate of bone formation.

By doing phlebotomy in recommended dorsal venous arch, certain amount of

alkaline phosphate is taken away can also be prevented by increased metabolism and

blood flow. In this way, phlebotomy in dorsal venous arch is beneficial. 93

VICHARCHIKA:

In Vicharchika, there is Rukshata developed in Hasta and Pada i.e. cracks like

associated with excess itching and pain. 61, 94

The condition Vicharchika Kushta may be correlated to ‘Eczema’95. It is one

of the type of skin disease, grouped under non-infectious inflammatory dermatoses.

The pathological term dermatitis is synonym with clinical term eczema. Both

dermatitis, eczema refer to inflammatory response to a variety of agents acting on the

skin from outside or from within the body.

In other words, a chronic relapsing pruritic skin condition of unknown

etiology with personal history and family history.

Predisposing Factors :

1. Chemicals

2. Drugs

3. Irritants

4. Unhygienic states

5. Photosensitivity.

Pathology :

This has been well studied that it is due to contact hypersensitivity. Initially

antigens at the epidermal surface are taken up by dendritic Langerhans cells which

migrate by the dermal lymphatics to draining lymph nodes. Antigens processed by the

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Langerhas cells are presented to ‘T’ cells. These ‘T’ cells migrate to affected skin

sites where they release cytokines and numerous inflammatory cells. There is local

cytokines release in the vicinity of dermal post-capillary venules. This results in

endothelial activation, where by endothelial cells become enlarged and express

molecules on their plasma membranes that promote adhesion of circulating T

lymphocytes. Once T cells enter the site of antigen through activated microvessels,

they elaborate large numbers of inflammatory cells to the site resulting structural and

functional integrity of epidermis.

There is acanthosis (thickening of epidermis due to hyperplasia of stratum

Malphighi). Loss of connection between epidermal cells with formation of

intraepidermal space containging odema fluid and detached epithelial cells. There is

thickening of horny layers. Intracellular oedema of the epidermis which may progress

to vesicles formation in the epidermis. Upper dermis shows crusts containing

degenerated leucocytes, bacteria and fibrin.

Morphological features :

1. Erythema

2. Odema

3. Papules

4. Oozing

5. Crusting

6. Fissuring

7. Scaring

8. Pigmentation

9. Thickening.

Critics :

In Vicharchika there is Rookshata developed in Pada. By means of blood

letting in the site two Angula above from the Kshipra Marma by Siravyadha is done

where Vata Gunas are neutralized. So the site may be considered for blood letting.

The condition may be correlated to ‘eczema’, where there is contact

hypersensitivity due to which there is hyperplasia of the skin. Epidermis is thick

containing a fluid in intraepidermal space. Upper dermis showing crusts containing

degenerated bacteria, fibrin. In general, structural and functional integrity is lost.

When blood letting by venesection is done in dorsal venous arch, venous drainage of

that part is improved, fresh blood is rushed providing oxygen and nutrients for proper

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growth epidermis layer. And also nor-epinephrine and epinephrine hormones are

released acting as an anti-allergic. Because, these hormones released in local tissue

areas cause local circulatory effects. So the site for Siravyadha may be considered.

PADADARI :

In persons who are in habit of walking too much, Vata becomes aggravated

produces dryness of sole cracks / fissures in the soles which is painful. This is known

as ‘Padadari’. 62, 96

This occurs in persons whose profession is to walk long distance daily or in

persons living in desert areas where there are no facilities of cars, buses etc. In India it

is very common in farmers, labour and villagers. In this, Vayu with its intense

Rooksha Guna, gets aggravated and produces cracks and fissures in soles of the feet.

This can be correlated to Rhagades or Crack or Fissure in Sole it is a vertical

loss of epidermis and dermis with sharply defined walls; crack in skin.97 Rhagades

gets aggravated in cold season and in very hot climate. Disease may constitutional in

some cases. The patient feels unbearable pain on placing foot on the ground. Pain is

reduced on wearing tight shoe and on massaging with oil or ghee on the cracked

portion of the sole of the foot.

Critics :

When Vata is aggravated causing dryness in Pada and also pain known as

Padadari. By Siravyadha two Angula above from Kshipra Marma, Rukshata of Pada

is relieved and pain is reduced. When it is correlated to ‘Rhagades’ or ‘cracks’. As

there is vertical loss of epidermis layer, blood letting by venesection of dorsal venous

arch will improve the venous drainage. Concurrently local tissue metabolism is

improved because of rush of blood and there is release of hormone.

SHLEEPADA:

Vataja Shleepada Chikitsa :

In Vataja Shleepada, after unction and sudation of the patient, the surgeon

should puncture the vein four fingers above the ankle. 63, 98

Pittaja Shleepada Chiktsa :

In Pittaja type, the vein located below the ankle, that should be puncture;

besides Pitta alleviating measures should be employed as in Paittika tumour and

erysipelas. 64, 98

Kaphaja Shleepada Chikitsa :

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In Kaphaja type, the physician should puncture the well know vein in the big

toe. 65, 98

Pada becomes Shila Saman Kathina, Sthoola ((Slivt` pd> Ål)pdm` ..)

called Shleepada.

Nidana: 66, 99

Stagnant water, Sheetala Ahara and Vihara and Anupa Desha are the causative

factors for Shleepada.

Samprapti: 67, 100

Nidana Sevana Kaphapradhana Tridosha Prakopa vitiated Dosha get

Ashraya in Vankshana, Uru, Janu, Jangha afterwards takes Ashraya in Pada

produces Ghana Shopha Shleepada.

Dosha Kapha Pradhana Tridosha

Dushya Rasa Dhatu

Sthana Padagata Lasikavahi.

Types It is of three types

(I) Vataja Shleepada Laxana :

(a) Krisha, Rooksha, Sputita Shotha

(b) Teevra Vedana

(c) Mild fever.

(II) Pittaja Shleepada Laxana :

(a) Peeta Sankasha

(b) Daha Jvarayukta

(c) Soft to touch

(III) Shlaishmika Shleepada :

(a) Shweta or Pandu Vrana

(b) Snigdha

(c) Guru

(d) Sthira

The condition can be correlated to filariasis.101 Filariasis is a global problem

where there is no satisfactory treatment. “Wucheraria bancrofti” and “Brugia mallai”

parasites are responsible for filariasis. The clinical course of the disease is

inflammatory. Presence of adult worms in lymphatic vessels induce obstruction or

mechanical blockage of the lymphatic channels, causing ‘lymphoedema’. The tissues

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surrounding the blocked lymphatics are infiltrated by chronic inflammatory cells such

as lymphocytes, plasma cells, eosinophills. Chronicity of process causes enormous

thickening and induration of the skin of leg.

Clinical Features :

Acute and Chronic :

Fever, lymphangitis, urticaria, regional lymphadenitis, epididymo-orchitis and

eosinophilia. Lymphoedema, non-pitting edema; skin is dry and thick, contours of

ankle is lost.

Critics :

Here in Shleepada, Kapha Pradhana Tridosha, Rasadhatu are involved where

Adhisthana is Uru, Janu, Pada. Usually it is due to stagnant water, where Kapha

Pradhana, Tridoshadusti takes place, Dosha get aggravated, resulting into Shotha

initially in Vankshana, Jangha, Janu gradually settled at Pada.

In the initial stages, Vata involvement is dominant and the condition may

occur in Vankshana. So Adhahjanghagat Siravyadha is done i.e. four Angulas above

from Gulfa Sandhi in Vataja Shleepada.

In Pittaja, the condition is descending down like Jangha, Janu, Adhahajangha

so Siravyadha is done in 4 Angula, below from Gulfa. Likewise in Kaphaja when the

condition settled down in Pada, the Siravyadha done in the site 4 Angula above from

Kshipra Marma.

By means of Siravyadha Dooshita Kapha and Rasa may be expelled out

neutralizing Shotha. So Siravyadha in particular site might have been dealt by

Sushruta.

When we have reviewed the pathology of filariasis, the obstruction

(mechanical blockage) of lymphatic channels causing lymphoedema. The surrounding

tissues are infiltrated by chronic inflammatory cells such as lymphocytes,

eosinophiles.

1/10th of interstitial fluid is drained by lymphatic channels. On the contrary,

interstitial fluid and lymph are similar but the difference is only location. Lymph

returns proteins from tissue spaces into blood. Through lymph only, certain bacteria,

toxins and other foreign bodies are removed from tissues. lymphatic capillaries are

slightly larger in diameters than blood capillaries. And has unique structure that

permits interstitial fluid to flow into them but not out. The endothelial cells make up

the wall of a lymphatic capillary overlap. When pressure is greater in the interstitial

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fluid than in lymph, the endothelial cells separate slightly like the opening of the one

way singing door and interstitial fluid enters the lymphatic capillary. When pressure is

greater inside lymphatic capillaries adhere more closely and lymph can not escape

back into the interstitial fluid.

On the basis of this physiology the venesection will definitely helpful in

filariasis. Because 1/10th fluid is drained by lymphatic capillaries. Wherever

lymphatic channels are blocked; the interstitial fluid is not drained by capillaries when

blood letting is done locally, the somewhat pressure in the lymphatic channels is

decreased and also as there is stimulation of endothelial cells they can cause relieve of

blockage also which may provide opening of lymphatic capillaries and also local

metabolism increased. So according to the condition of situation of swelling

Siravyadha site is selected, So that, four Angula above from Gulfa is long saphenous

vein and tributaries at the junction of upper two third and lower one third of the leg.

Likewise if Shotha is there in Pada, short saphenous vein, dorsal venous arch blood

letting is done.

KROSTUKASHIRSA :

In Kroshtuka Sirsha, Khanja, Pangu and pains produced by Vata, puncturing

should be done in Jangha, four Angula (8 cm) above the ankle joint. 68, 102

As per the above said treatment Siravyadha is done in the said diseases, four

Angulas is done in the said diseases, four Angulas from the Gupha Sandhi. The

anatomical location of vein of that part is interpreted on available anatomical basis. In

Gulpha Sanhi, the Gulpha Marma is located, so, Siravyadhana is done above from the

the Gulpha Marma 103 by protecting the Marma Sthana.

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TABLE NO. 8 SHOWING DETAILS OF GULPHA MARMA

Measure and

Type -

2, Sandhi, 2 Anguli

Site -

Ankle joint and the tibia as well as calcium bone. Controls

Medovaha, Asthivaha, and Shukravaha Srotas

Tissue involved

Anatomical

structures

-

Flexor hallucis longus and brevis, tibialis posterior and flexor

or digiti longus muscles. Posterior tibial nerve. Posterior tibial

artery and vein.

Sign if injured

-

Injury to the joint will cause swelling with impairment of the

functions of flexion, extension etc. It is Vaikalyakara type of

Marma

Treatment

-

Suchi Karma (acupuncture) – For tubercular knee, sever pain

in the groin, paresis of the leg, paralysis of the leg, it should

be done, 4 Anguli above the Marma.

As the site of Vyadhana is Gulpha, that area is drained by long saphenous vein

and its tributaries. It starts on medial border of the foot and passes upwards just

anterior to the medial malleolus. It is very consistent in position at this point and can

usually be easily identified as a site for vein harvest.

The long saphenous vein can often be seen as it runs upwards and backwards

across the medial surfaces of the tibia is little above and in front of the medial

malleleolus. This is a useful site for obtaining surgical venous access.

The long saphenous vein is very prominent and easily marked at the medial

border of the tibia at the junction of the upper two third and lower one third of the

leg.104

In Janusandhi, Vata and Rakta Vikruti leads to pain in the knee joint and

swelling which looks like head of fox.69, 105

The condition can be correlated with Septic Arthritis.106 That is Inflammatory

involvement of the joint due to infectious agents like streptococcus, staphylococcus.

Precipitating Factors :

(1) Immunosuppressive therapy (2) alcoholism (3) drug abuse (4) chronic

arthritis.

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Pathology :

There is direct hematogenous seeding of synovium. The large joints of

extremities are commonly affected (75% knee joints). The synovium is well

vascularized and lacks a limiting basement membrane. The process begins with

hyperaemia, synovial swelling and infiltration by polymorphonuclear and

mononuclear leucocytes along with the development of effusion in joint space. There

may be formation of inflammatory tissues and onset of fibrous affections between the

opposing articular surfaces resulting in permanent ankylosis. And also there is release

chondrolytic enzymes contribute to destruction of articular cartilage.

Clinical Features :

1. Pain

2. Warmth

3. Swelling

4. Restricted movement

5. Co-existence of Rheumatoid arthritis

Critics :

In Janusandhi, Vata and Rakta Nirukti leads to pain in the knee joint and

swelling looks like head of the fox. There is involvement of Vata and Rakta. here is

also letting is done in same site where in Vataja Shleepada is done, i.e. 4 Angula

above from Gulfa. By means of Siravyadha Raktamokshana, Dooshita Rakta may be

expelled out and Vata Margavarodha is relieved. So Sushruta might have told this site

for Siravyadha in Krostukasheersha.

As the condition is similar to that of septic arthritis, by means of blood letting

by phlebotomy in long saphenous vein the hyperuriaemia is relieved, by release of

steroid hormone. The effusion (swelling) is resolved. Fibrous adhesions are relieved.

In this way blood letting may help in septic arthritis. So the particularly site told by

Sushruta can be considered.

KHANJA :

Prakupita Vata is getting Ashraya in ligaments of the limbs, causing an

individual to incapability to walk is called Khanja. 69, 107

This condition can be correlated to Monoplegia or poliomyelitis. This is usually due

to lower motor neuron disease with or without associated sensory involvement. Upper

motor neuron weakness occasionally presents with a monoparesis of distal and non-

anti-gravity muscles (LMNL).108

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Poliomyelitis :

Much of what is known about the pathogenesis of enteroviruses has been

derived from studies of Polio virus infection. After ingestion, Polio virus is thought to

infect epithelial cells in the mucosa of the gastrointestinal tract and to spread to and

replicate in the submucosal lymphoid tissues. The virus next spreads to the regional

lymph nodes, and viraemia phase ensues and viruses replicates in organs of

reticuloendothelial system. In some cases, a second viraemia occurs and the virus

replicates further invasions of tissues, sometimes causing symptomatic disease. It is

uncertain whether polio virus reaches the CNS during viraemia or wheather is also

spreads through peripheral nerves.

Enterovirus have worldwide distribution.

Clinical Features :

1. Incubation periods 3 to 6 days

2. The common presentation is paralytic disease

3. Severe back, neck and muscle pain by rapid development of motor weakness.

Critics :

In Khanja, Katisthith Prakupita Vata getting Ashraya in Khandaras of Sakthi

resulting into Khanja where there incapability to walk because of single limb

deformity.

Usually because of Margavarodha the Vata got vitiated when Siravyadha is

done in recommended site i.e. four Angula above from Gulfa (long saphenous vein),

Margavarodha is relieved when Vata may get neutralized.

The condition can be correlated to monoplegia which is usually lower motor

neuron lesion. Blood letting by phlebotomy may help locally and systemically also.

Because if there is any thrombus that will be dissolved by fibrinolytic activity of

blood letting. And locally by blood letting removal of waste products of cellular

metabolism is improved and various hormones are released to maintain homeostasis.

Nerve stimulation can occur. So in particular site, Siravyadha may be told by

Sushruta.

PANGU :

Prakupita Vata is getting Ashraya in ligaments of the limbs, causing an

individual to incapability to walk is called Pangu. 71, 109 This condition can be

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correlated to diplegia or paraplegia. Cerebral palsy carries connotation of a

development disorders of motor function, that is present from infancy or early

childhood and that is due to non-progressive cerebral disorders. The most commonly

encountered condition is spastic diplegia (affecting both legs).

Cerebral infarction resulting from hypoxia or ischaemia is one determinant of

these disorders, for most abnormal state has its origin before birth in events that go

unrecognized. The insult may occur perinatally as a result of obstetrical mishap. For

some people encephaloclastic event occurs in early childhood.

Pathology :

Ischaemic necrosis in the brain results from ischaemia caused by considerable

reduction or complete interruption of blood supply to the neural tissue which is

insufficient to meet its metabolic needs. The brain requires sufficient quantities of

oxygen and glucose so as to sustain it’s aerobic metabolism, mainly by citric acid

cycle i.e. Kreb’s cycle which requires oxygen. Moreover, neural tissue has limited

stores of energy reserves so that cessation of continuous supply of o2 and glucose for

3-4 minutes results in permanent damage to neurons and neurological cells.

Deprivation of o2 to the brain may occur in 4 different ways.

1. Anoxic – where there is low inspired Po2

2. Anaemic anoxia – in which o2 carrying haemoglobin is reduced.

3. Histotoxic anoxia – e.g. cyanide poisoning

4. Stagnant anoxia – in which the damage is caused by cessation of blood with

resultant local accumulation of metabolites and changes in pH

In all these different forms of anoxia the end results is ischaemic brain

damage, which may be of two manners – (i) generalized cerebral

hypoperfusion (ii) localized reduction of blood supply.

The brain receives 20% of cardiac output for maintaining its vital aerobic

metabolism. Various factors are responsible for irreversible ischaemic damage, such

as body temperature hypoxic episodes pre-existing cerebral diseases. Normally, brain

continues to be perfused upto arterial pressure below this critical value results, rapid

fall in cerebral perfusion. The pathological appearance of the brain varies depending

upon the duration and severity of hypoxic episode. Microscopically, nerve cells die

and are replaced by reactive fibrillary collagenous tissue.

Critics :

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The condition ‘Pangu’ is same as that of Khanja. But both legs are involved.

Prakupita Vata getting Ashraya in Sakti Kandara, Sira, Snayu, Nadi etc. So

Raktamokshana by Siravyadha at 4 Angula above from Gulpha may cause

neutralization of Doshas. So the local Raktamokshana is dealt.

The condition can be correlated to diplegia, where cerebral palsy of

developmental disorder of motor function. Cerebral infarction resulting from hypoxia.

When there is considerable reduction in blood supply to neural tissue which is

insufficient to meet its metabolic needs. The brain requires sufficient o2 and glucose

so as to sustain metabolism.

Cerebrum is most vascular area of the brain. It is highly related to metabolism

of cerebral tissue. Metabolic factors have potent effect in controlling cerebral blood

flow. They are nothing but co2, hydrogen ion and o2. An increase in co2 or hydrogen

ion concentration increases the cerebral blood flow, where as decrease in o2 increases

the blood flow. By means of dilating the cerebral blood vessels increases the blood

flow, which inturn carries co2 and acidic substances. Oxygen deficiency also increases

the cerebral blood flow. On the basis of this theory, as blood letting in long saphenous

vein may induce higher co2 and hydrogen ion concentration which in turn cause

dilatation of cerebral blood vessels with increased blood flow. Concurrently it is

carrying away the acidic substances from the neural tissue.110

APACHI :

In Apachi, Siravyadha is done at two Angula (4 cm) below the Indrabasti

Marma. 72, 111

In above said disease, the Siravyadhana is done 2 Angula below the

“Indrabasti Marma”. The anatomical location of the vein of that part is interrupted on

the available anatomical basis. Venesection is done 2 Angula below the Indrabasti

Marma in lower part of the back of leg. Here the small saphenous vein is easily

visible and usually it is the choice for the venesection.

TABLE NO. 9 SHOWING DETAILS OF INDRABASTI MARMA

Measure and Type - 2, Mamsa, ½ Angulas Site - The point at the middle of the line, joining the posterior

surface of the calcaneum with the centre of the popliteal

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fossa. Controls Agni, small intestine and Annavaha Srotas Tissue Involved and Anatomical structure

- Gastronemics, soleus and plantaris muscles. Peroneal (branch of posterior tibial) and posterior tibial artery and vein. Drainage of lymph to the popliteal lymph glands. Posterior tibial nerve.

Signs if injured - Injury may cause impairment of the function of the foot. If the artery is damaged, there will be severe bleeding, shock and collapse. It is Kalantara Pranahara type of Marma. (At this vital point, posterior tibial artery is more important than any other muscle or ligament)

The Sthana of Siravyadha is two Angula (4 cm) below the ‘Indrabasti Marma’.

This region comes back side of the leg. Here the Vyadhana is done by protected

Marma and its structure. So it is mentioned that venesection is done below the vital

spot. This area is drained by small saphenous vein, usually it can be selected for

venesection, as this vein is easily visible in its lower part.

The short saphenous vein begin at the lateral aspect of the dorsal venous

arches of the foot, cause along the back of the leg. It is the continuation of the lateral

marginal vein. In the lower third of the calf it ascends only by superficial fascia and

skin. It is easily marked at the point behind the lateral malleolus and just lateral to the

tendocalcaneus above the lateral malleolus it drains the lateral border of the foot, the

heel, and the back of the leg. It is connected with the great saphenous vein at the

middle of the calf region by accessory saphenous vein.

It receives many cutaneous tributaries in the leg. In leg, small saphenous vein

ties near the sural nerve.112 Usually short saphenous vein at lower third of the back of

leg is selected for venipuncture.

Nidana :

Since there is no direct explanation of Nidana of Apachi, Dosha involvement

is considered as Kaphadusti and Meda-dusti. So the factors vitiating Kapha and Meda

are responsible for Apachi. 113

Samprapti :

Kapha and Meda are accumulated in Hanvasthi, Akshikasthi, Bahu, Jangha,

and Manya producing Granthis. They are stiff, round, circular, painful, resembling

seed of Amalaki and Matsyanda Jala.

Dosha Involved :

Dosha : Kapha pradhan Tirdosha

Dushya : Meda

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This condition can be correlated to Lymphadenitis which is an inflammatory

condition of lymph nodes.

Etiologies :

1. Inflammatory

2. Infective

3. Neoplastic

Pathology :

Lymph nodes undergo reactive changes in response to a acute variety of

stimuli which include microbial infections, drugs, tissue injury, neoplasia. The

affected lymph nodes are enlarged three times to their normal size. Microscopically,

sinusoids are congested widely dilated and edematous. But in chronic course lymph

nodes are enlarged, firm, non-tender.

Clinical features :

Firm, movable, round, swelling in all regions of the lymph nodes.

Critics :

Where in Apachi, Kapha Pradhana Tridosha and Meda are involved resulting

in Granthi Samana Shotha called Apachi. If it may occur in Manya, Bahu, Jangha etc,

where ever it is situated in upper or lower extremities, Siravyadha is done 2 Angula

below from Indrabasti Marma. Where there is neutralization of Doshas and

mobilization of Medas, so particular site is selected. As per modern science is

concerned lymphadenitis, that is nothing but reactive changes in response to any

stimuli like infections, injury, drugs, neoplasms. As these are connected to the

channels, lymphatic circulation is meant for drainage of toxins and bacteria engulfed

by lymph nodes causing as lymphadenitis. By means of the blood letting venous

drainage is improved. Automatically, lymphatic drainage is improved resolving

inflammation of lymph nodes by increased blood flow, metabolism and removal of

waste products from the interstitial space. So, local part is selected for Siravyadhana

at median vein in upper limb and short saphenous vein in lower limb.

GRUDHRASI :

In Grudhrasi, it should be done four Angula (8 cm) either above or below the

knee joint. 73, 114

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As per above said quotation the Siravyadha is done, four Angula (8 cm)

Sandhi, Janu Marma 115 is located. So, by protecting the vital point Siravyadha is done

below the Janu Sandhi.

TABLE NO. 10 SHOWING DETAILS OF JANU MARMA

Measure and Type - 2, Sandhi, 8 Anguli Site - On the knee joint, Right Marma controls liver, left

Marma controls spleen. Tissue Involved and Anatomical structure

- Knee joint, posterior cruciate ligament, olique posterior ligament, plantaris and gastronemis muscle. Popliteal artery and vein, femur, tibia and patella bones. Medial popliteal nerve.

Signs if injured - Injury to the knee can cause severe pain, edema, difficulty in walking, disfigurement and impairment of all the functions of the joint. It is Vaikalyakarama type of Marma

Treatment - Agnikarma – In sciatica, as usual select sensitive joint 4 Angulai proximal or distal to the Marma and apply heated gold probe at the point.

Usually the great saphenous vein is easily found in this area for venesection

i.e. four Angula below the Janu Sandhi. It begins on the medial side of the dorsum of

the foot and runs upwards and backwards anterior to medial malleolus and then to the

medial surface of the distal third of the tibia. It then ascends on the medial border of

the tibia to the postero-medial surface of the knee and inclines anteriorly through the

thigh to enter the femoral vein. The vein has several communication through the deep

fasica with deep veins. Just below the knee, this vein communicates with anterior vein

of the leg.

When Kandaras of Parshni Padangulis are vititated by Prakupita Vata then

contraction-relaxation of the limb is restricted called “Grudhrasi”. 74, 116

Nidana :

Sheeta, Rooksha – Ahara, Ati-jagarana, Ati-maithuna, Ati-malapravrutthi, Ati-

Shrama, Dhatuksheenata, Chinta, Shoka, Krodha, Amadosha etc.

Samprapti and Laxanas :

Because of above Hetus vititation of Vata results from Sphik, raditating to

Kati, Prushta, Uru, Janu, Jangha, Vedana. Usually, pricking type of pain exists often

Spandana is felt in these areas. If there is involvement of Kapha there is presence of

Tandra, Jadata, Aruchi. Vagbhata considers Grudhrasi as similar to Vishwachi.75, 117

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This is correlated to Sciatica 118 which means pain in the distribution of sciatic nerve

and its components nerve root. Instead as a disease is accepted as lumbar disc

prolapse, which is a common cause of low back ache.

Etiologies :

1. True sciatica neuritis is leprosy, trauma, post-herpetic neuralgia.

2. Mechanical pressure nerve roots

3. In vertebral column – Fibrocytis

4. Lumbar disc diseases

Clinical features :

1. Pain felt in buttocks radiates down the posterior aspect of the thigh, calf, outer

border of foot.

2. Increased on coughing, sneezing, and excess of walking

3. Parasthesia along the nerve root

4. Calf muscle weakness

Critics :

Because of Prakupita Vata, contraction, relaxation of limb is restricted

resulting into pain from Sphik radiating to Kati, Uru, Janu, Jangha etc. By means of

Siravyadha four Angula above or below Raktamokshana is done, where Vatadushita

Rakta is expelled out and pain is relieved. If the intensity of pain is in Prusta, Kati,

above site is selected, if its intensity is more in Pada, below site is selected. In

sciatica, similar features can seen, where in there is compression of sciatica nerve due

to various causes like unusual stretching, neuritis, fibrositis, lumbar disc prolapse etc.

So there is shooting pain along with distribution of sciatic nerve. Usually pain is

associated with tissue damage, free nerve endings are the pain receptors. There may

be various stimuli like mechanical, chemical, thermal causing pain. This is considered

as mechanical. So that because of compression of nerve, blood supply to the tissue is

blocked, then tissue becomes painful. Pain during blockage of blood supply is due to

accumulation of large amount of lactic acid in tissue. Certain chemical agents formed

such bradykinin and proteolytic enzyme which stimulate at nerve endings. So in any

nerve compression or muscle spasm, there is pain but by means of blood letting,

branch of great saphenous vein, 4 Angula above or below, blood flow to the

compressed part may be increased by angiogenesis, as much as possible aerobic

metabolism is enhanced, where the accumulation of lactic acid can be prevented and

accumulated lactic acid may be drained. By means of blood letting the hormone

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serotonin is released, believed to cause presynoptic and postsynoptic inhibition,

avoiding pain. So if the pain is situated in back and thigh, then upper site is selected,

if the pain is radiated upto leg, lower site is selected.

GALAGANDA :

In Galaganda that vein present at the root of the thigh should be punctured.

This description is also applicable for opposite Shakti and in both Bahus. 76, 119

In Galaganda, aggravated Vata and Kapha Doshas in Gala Pradesha get

Ashraya in Majja and Meda and then produce symptoms according to their Dosha

dominancy. 77, 120

Types :

1. Vataja Galaganda

2. Kaphaja Galaganda

3. Medaja Galaganda

Laxana :

1. Mushkavat – Shotha in neck region

2. Mobile or immobile Galaganda

3. Cold, smooth in nature

4. Improper speech

5. Difficulty in breathing etc.

This can be correlated to Goitre, the term ‘goitre’ is defined as thyroid

enlargement caused by compensatory hyperplasia and hypertrophy of the follicular

epithelial in response to thyroid hormone deficiency. The end result of this

hyperplasia is generally euthyroid state which may be hypo or hyper thyroidism.

Goiter is of two types – 1. simple non-toxic 2. multinodular – toxic.

Pathogenesis :

The mechanism of both the forms of goiter can be considered together, since

nodular goiter is generally regarded as end stage of long standing simple goiter.

Deficient production of thyroid hormone due to various factors. Most common causes

dietary lack of iodine. Deficient thyroid production causes excessive TSH stimulation

which leads to hyperplasia of follicular epithelium as well as formation of new

thyroid follicles. Cyclical hyperplastic stage followed by involution, leads to simple

goiter. Repeated and chronic changes of hyperplasia result in continued growth of

thyroid tissue while involuted area undergo fibrosis leads to nodular goiter. 121

Critics:

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In Galaganda, Urumula Samsthita Siravyadhana is done, where there may be

neutralization of Kapha-Meda-Rakta Dusti. Any relevance cannot be interpreted or

elicited here. On the contrary, if that is correlated to goiter, which is hyperplasia of

follicular epithelium of thyroid follicles where there may gradually growth of thyroid

tissue and fibrosis. Probably the condition tends towards non-toxic goiter i.e.

hypothyroidism. Here, blood letting by phlebotomy may help by many ways. It may

directly stimulate pituitary to release TSH. Indirectly improve metabolism of whole

body by release of numerous chemicals and hormones. As the available veins of neck

and abdomen are contraindicated for Siravyadhana, so Urumula Sthita Sira may

accepted for Siravyadha.

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TABLE NO. 11 SHOWING SITES FOR SIRAVYADHA OF DIFFERENT

VYADHANA STHANAS PARTICULAR DISEASES IN LOWER LIMB

Sl. No. Vyadhis Vyadha Sthanas (I).

1. Padadaha 2. Padaharsha 3. Visarpa 4. Chippa 5. Vatarakta 6. Vatakantaka 7. Vicharchika 8. Padadari

Two Angulas (4 cm) Above the Kshipra Marma

(II). 1. Vataja Shleepada Four Angula above the

“Gulfa Sandhi 2. Pittaja Shleepada Four Angula below the

“Gulfa Sandhi 3. Kaphaja

Shleepada Four Angula above the “Kshipra Marma”

(III). 1. Kroshtukashirsha 2. Khanja 3. Pangu

Four Angula above from ‘Gulfa Sandhi’

(IV) Apachi Two Angula below from ‘Indrabasti Marma’

(V) Gridhrasi Four Angula above from ‘Janu Sandhi’

(VI) Galaganda Urumoola Sthita Sira

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(II) URDHVASHAKHAGATA VEDHYA SIRA STHANAS : [Fig. 9]

Pleehodara:

In diseases of Pleeha, puncturing should be done especially in the left arm

either at the inner side of elbow joint in the centre of arm or in the are between the

little and ring fingers. 78, 122 As per above information in Pleehodara Siravyadha is

done in left sided Kurpara Sandhi Sthita Sira i.e. median cubital vein which is situated

above ‘Kurpara Marma’.123 It is a type of Sandhi Marma controlling Raktavaha

Srotas, so that Marma on right controls liver, Marma on left controls spleen.

The prominent medial cubital veins links cephalic and basilic vein. It receives

number of tributaries from the front of forearm and gives off the median vein, which

pierces the facial roof of antero-cubital fossa to join the venae commitants of brachial

artery. So the vein recommended for Siravyadha may be left sided medial cubital

vein.

Or otherwise vein situated in between little finger and ring finger may be used

for Siravyadha. As per context, it may dorsal venous arch lies on the dorsum of the

hand. Its tributaries include dorsal metacarpal veins, dorsal digital veins from the

medial side of the little finger and dorsal digital from the index finger two dorsal

digital veins from the thumb. 124

Because of consumption of Adhika Vidahi, Abhishyanda, Ushna, Lavana,

Gunatmaka, Ahara and Vihara Sambandhi Atiyana, Atichinta, Ativyayama, lifting

heavy weights, improper Panchakarma therapy. 79, 125

Samprapti :

Due to above said causes there is a enlargement of spleen which we call it as

Pleehodara especially on the left side. Dosha involved is Kapha, Dushya is Rakta,

Adhisthana – Pleeha, Srotas – Rasavaha and Raktavaha.

Laxana :

Mandajvara, loss of appetite, indigestion, anaemia, loss of strength.

This can be correlated with Splenomegaly.126 Enlargement of spleen can be an

important diagnostic clue of the underlying disorders, when it is sufficiently enlarged

that causes protuberance on left side and dragging pain in left upper quadrant.

Usually spleen is a large single mass of lymphatic tissue in the body with

multiple functions like formation of blood cells, destruction of blood cells, reservoir

function and role in defense mechanism.

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Etiologies :

1. Infection conditions like malaria, enteric fever, viral hepatitis, tuberculosis,

syphilis.

2. Autoimmune diseases like R A, thrombocytopenia.

3. Altered blood flow to the spleen.

4. Cirrhosis of liver.

5. Portal venous obstruction.

6. C C F

The other rare diseases splenomegaly is seen.

Pathology :

Enlarged spleen is heavy and firm. The capsule is tense and thickened. There

is dilatation of sinusoid with prominence of splenic cord. The white pulp is atrophic.

Critics :

Because of the involvement of Kapha, Rakta, Rasavaha, Raktavaha Srotas,

there is enlargement of spleen resulting into mild fever, loss of appetite, indigestion,

weakness etc. By means of blood letting in Vama Kurpara Sandhista Sira, Rasavaha,

Raktavaha Srotoshodhana can occur and Kapha-Raktadusti is neutralized, resolving

Pleehodara. That is the Sthanika Raktamoksha from the nearest vein of the spleen

(Vama Kurpara Sandhisthita Sira). The condition may be similar to spleenomegaly. In

spleen more than 100 ml of blood is always reserved. Spleen has got turn separate

areas for storage of blood, venous sinuses and pulp. Small vessels flow directory into

venous sinus cause sinuses to swell up. The red cells are expelled by spleen into

general circulation. Blood passing through spleen pulp, before it enters the sinuses

under goes through squeezing. So it is expected that RBC’s would not withstand the

trauma. So many of RBCs destroys in the body have their final demise in spleen.

After cellular rupture, the released hemoglobin through the cell trauma are ingested

by reticuloendothelial cells of the spleen, when blood is invaded by infectious agents,

the reticuloendothelial cells of the spleen are rapidly remove the debris, bacteria,

parasites. Due to any cause when there is spleenomegaly, phlebotomy done in left

medial cubital vein by which reserved blood in the spleen is ejected into general

circulation, so that fragile RBCs are wased off, fresh RBCs are formed, blood

circulation to the spleen is increased, so there is removal of old cells. Splenic vein is

drained effectively, so blood letting in left median cubital vein is done in

splenomegaly.127

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YAKRIDLYUDARA:

In Yakrudalyudara, puncturing should be done especially done in the right arm

at the same space. 80, 128

As per above said quotation in Yakrudotodara and Kaphodara, Kasa Shwasa

Siravyadha is done is right sided ‘Kurpara Sandhisthita’, it is right median cubital

vein, which is situated above Kurpara Marma. It is a type of Sanhi Marma controlling

Raktavaha Srotas, so that it controls functions of liver and spleen.

The prominent median cubital vein links cephalic and basilic vein. It receives

number of tributaries from the front of the forearm and gives off the median vein,

which pierces the fascial roof of anterior cubital fossa to join the venae commitantsof

brachial artery. So the vein recommended for Siravyadha may be right sided medial

cubital vein.

The word ‘Dalana’ means laceration and ‘Bhedana’ means ‘cleavage’ or

splitting. So it becomes apparent that a pathological condition in which ‘Yakrit’ gets

structurally damaged by continued cleavage due to vitiated Doshas especially Rakta

and Kapha, where it often enlarges the liver called “Yakridalyudara”.

Nidana :

1. Excessive intake of Vidahee and Abhishyandi Ahara are the main aetiological

factors of Yakridalyudara.

2. Riding on the animals, vehicles, after taking food causing aggressive

movements of the body.

3. Excessive hard work, excessive and walking, lifting heavy weights.

4. Apart from the above, the quantitative and qualitative vitiation of Rakta

Dhatu is also focused to cause ‘Yakridalyudara’.

Samprapti :

Due to above said pathological factors ‘Rakta’ and ‘Kapha’ get vitiated which

cause Vriddhi of Yakrit called Yakriddalyudara.

Charakacharya stresses on the point that, Yakrit Sthana-chyuti or Vriddhi is

taking place as there is gradual vitiation of Rasa and Rakta. He says further that the

‘Yakritvriddhi’ is Kathina like Astheela in later stages and gets the shape of tortoise

shell in advanced stage.

Laxana :

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1. Yakrit Vriddhi

2. Manda Jvara

3. Pandu

4. Mandagni

5. Aruchi

6. Mutraghata

7. Angamarda

8. Moorcha.

Types :

1. Vataja

2. Pittaja

3. Kaphaja

4. Sannipataja

5. Raktaja

Vataja, Pittaja, Kaphaja and Sannipataja are Aushadha Sadhya and Raktaja –

Shastrasadhya. 129

Usually liver is an important solid organ where different chemical reactions

are taking place and acts a blood reservoir, whatever the etiological factor that causes

enlargement of liver is called hepatitis which may correlated to Yakrudalyudara.

Aetiologies :

1. Viral (Hepatitis B)

2. Bacterial

3. Chronic alcoholism

4. Metabolic disorder like hypolypedaemia

5. Hepatotoxic drugs

Pathology :

The liver enlargement takes place in three different stages.

1. Fatty liver : As liver acting on a metabolism of the fatty acids,

macroscopically liver looks like pale or light yellow and feels like greasy.

Hepatocytes are enlarge 2-3 times of their normal diameter. The enlargement

of hepatocytes is not only lipids but also increase in their protein and water

content. Often the mitochondria are dilated and distorted. Sever fatty change

leads fibrosis where there is thickening of wall of some central hepatic vein.

Sometimes minor fibrosis around terminal hepatic vein.

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Clinically, it goes undiagnosed later there may be features like

epigastric pain, nausea, vomiting, jaundice and non-tender hepatomegaly.

2. Hepatitis : It is nothing but greater extent of hepatocellular necrosis. Usually

injuries are greater in terminal hepatic vein. Because oxygen tension is

decreased in this part of the liver. And most of enzymes are active in the

hepatocytes around the hepatic veins.

Sometimes, hepaticytes are ballooned and shrinked. Mitochondria are

swollen and distorted. Mitochondria are commonly found in hepatocytes

around central hepatic vein. The adventitia of the terminal hepatic vein is

edematous. As fibrosis developed around terminal hepatic vein narrows or

occludes them.

Clinically, anorexia, nausea, vomiting, fever, fatigue, abdominal

discomfort, tender hepatomegaly, raised SGOT and SGPT levels.

3. Cirrhosis : Liver becomes shrinkened with abnormal architecture. Because of

continues necrosis replaced fibrosis resulting into fibrosis. Collagenous septa

is irregular around the terminal hepatic vein. Clinically anorexia, weightloss,

weakness, malnourishment, jaundice, malnutrition, oesophagial and rectal

bleeding firm hepatomegaly and gynecomastia. 130

Critics :

Because of involvement of Kapha and Raktadusti, there is right upper

abdominal swelling called Yakrutalodara. The Raktamokshana is done in Dakshina

Kurpara Sandhisthita Sira, it has to resolve Rakta and Kapha Doshas. The condition

can be correlated to ‘hepatomegaly’. The blood letting helps to mobilize the fatty

acids deposited in the liver by the secretion of steroid hormones. Liver congestion is

decreased, portal venous tension is decreased. Enzymatic activity of hepatic cells is

increased resulting appetite, lack of nausea, fever etc. Providing the production of

fresh RBCs which are not fragile but active and living their normal life span,

performing their normal functions. In this way phlebotomy in right medial cubital

vein has got direct effect on liver.

KAPHODARA :

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Kaphodara is a type of Udara, where predisposing factors are Avyayam,

Divasvapna, Adhika Madhura, Picchila, Dadhi, Dugdha Sevana. Avruta Vata

involving Kapha resulting into enlargement of abdomen outside the intestines.131

Here Laxanas like Aruchi, Angashoonata, Hastapada, Andakosha, Uru,

Shotha, Utklesha, Nidradhikya, Kasa, Shwasa. This condition may be correlated to

obesity. Obesity is nothing but the accumulation of fat in the body. When greater

quantity of energy in the form of food, enter the body than the expenditure, the body

weight increases. The precursor fat cells develop form a fibroblast like cell. The

enzyme glycoprotein lipase is detected in this cell type. Excess fat is associate with

hypertrophy of cell and hyperplasia. Abdominal obesity is more highly correlated

with metabolic complications. The pattern of abnormal adipose tissue development

can be altered by many changes. As the most of fat metabolism is done by liver. In

any impaired liver functions fat embolism is also impaired. 132

Critics :

In Kaphodara also Dakshina Kurpara Adhisthita Sira Siravyadha is done like

Yakrutodara. There is also involvement of Kapha, Rakta, Meda giving rise to

Kaphodara. Raktamokshana by Siravyadha helps in neutralizing Doshadusti.

When the same condition is correlated with obesity and the features are similar

to that of obesity. Where in obesity blood letting from right medial cubital vein helps

to mobilize fatty acids. As they help to improve the hepatocellular function. They

release certain enzymes of fat metabolism. So that might be the site dealt by the

Sushruta may be considered.

KASA ROGA :

Prakupita Pranavata is coming out through mouth producing a sound as if fall

of an utensil called Kasa. 81

Samprapti :

Bahya Nidanas (Dhoomopaghatadi) Pranavaha Srotas Khavaigunya and

Galasrotas Vataprakopa Pranavayudusti Nirgamana from Mukha Shuska

Kasa or Ardra Kasa. 133

Dosha: Dooshya Adhisthana :

Dosha : Vata Pradhana Kapha

Dooshya : Rasa, Swarayantra

Srotas : Rasavaha, Pranavaha

Adhisthana : Urah, Kantha

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Srotodusti : Shotha, Sanga

Kasa is nothing but cough, which is reflex action as defense mechanism, may

be due to many causes. Ex : URI, CRI. Whenever there is any vitiation is respiratory

tract then there is cough.

Critics :

Here, Dakshina Kurpara Sandhisthita Siravyadha is done where Sanga in

Pranavaha Srotas may relieved and vititated Doshas may be neutralized. So Dakshina

Kurpara-Abhyantara Sthita Siramokshana is done.

When the site is correlated according to modern medicine. That right medial

cubital vein where pressure is venous tension is decreased pulmonary congestion may

be relieved.

SHWASA :

Urdhvagati of Vayu with Vega is called Shwasa, caused by Vata-Kapha

Prakopaka Ahara-Vihara.134

Samprapti :

By means of Mithyahara-vihara, Prakupita Pranavaha leading to its normal

function, associated with Kapha to cause Shwasa with efforts. 135

The condition may be leads to emphysema, CCF or hyperuraecemia.

By means of phlebotomy in medial cubital vein, the congestion of lungs and

liver is relieved blood flow in necessary fact is increased metabolism is maintained.

So it many help in above conditions. Here the Sushruta’s verdict can be accepted.

VISHWACHI :

When Prakupita Vata involves Bahu, Prushta, Hasta, Tala and Anguli-

Kandaras, then there is Karma Kshaya of Bahu. 82, 136

In Vishwachi (pain in the arms) will be similar to that of Grudhrasi, so four

Angula above or below the Kurpara Sandhi Siravyadha is done.

In Vishwachi Raktamokshana is done four Angula from Kurpara Sandhi

nearer to Bharvi (Urvi) Marma, which is controlling the healthy tissue growth,

Rasavaha, Udakavaha Srotas. Regarding the vein of the site four Angula above from

the Kurpara Sandhi may be basilic vein, which is a post-axial vein of upper limb, that

begins with the dorsal venous arch, runs upwards along the medial border of the

forearm. Ends around the elbow where it pierces the deep fascia and lastly runs

around the medial side of the brachial artery.

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The site of Siravyadha may be four Angula below from the Kurpara Sandhi. It

is nothing but cephalic vein that begins from the lateral end of the dorsal venous arch.

It runs upwards winds around the lateral border of forearm, continues upwards along

the lateral border of biceps. It pierces deep fascia of pectoralis major. It pierces the

clavipectoral fascia and joints of axillary veins. 137

This is correlated to Brachial Plexus Neuritis. 138 Pain from the injury to the brachial

plexus of the arm can occasionally mimic pain of cervical origin.

Causes :

1. Neoplastic infiltration Ex: Ca breast

2. Horner’s syndrome

3. Infection by immunization

4. Pancost’s tumor of lung.

Symptoms :

1. Shoulder pain radiating down the arm

2. Numbness of the finger

3. Weakness of muscles, innervated by ulnar median nerve

4. Shoulder pain followed over weeks. By weakness of the proximal arm and

shoulder girdle muscle innervated by the upper brachial plexus

5. Muscle wasting and weakness resulting into flexion deformity.

Critics :

There is involvement of Vata, Which may effect Bahu, Hasta, Tala, Anguli,

when blood letting is done four Angula above or below Kurpar Sanhi, Vata may be

neutralized, giving strength to Kandaras. The condition is similar to brachial plexus

neuritis, where there is pain in arm, numbness in fingers, weakness of muscle,

shoulder pain, muscles wasting with flexion deformity.

Locally when blood letting is done in basilic vein, the pain precipitating

factors like lactic acid are reduced, blood supply to the brachial plexus is improved,

where there is aerobic metabolism in the part. There is provison of release of

serotonin also, which inhibits pain of neuritis. In this way blood letting site may

accepted.

TABLE NO. 12 SHOWING SITES FOR SIRAVYADHA OF DIFFERENT VYADHANA STHANAS PARTICULAR DISEASES IN UPPER LIMB

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Sl. No. Vyadhis Vyadha Sthanas (I) Pleehodara Vama Kurpara Sandhisthita Sira

or Sira present in between left Kanishtika and Anamika Angulas

(II) Yakrudalyudara Kasa Shwasa

Dakshina Kurpara Sandhisthita Sira or Sira present in between right and Kanishtika and Anamika Angulis

(III) Vishwachi Four Angula above the ‘Kurpara Sandhi’

(IV) Apachi Two Angula below from ‘Indrabasti Marma’

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1. VENOUS SYSTEM

Veins are characterized by relatively thin wall and large capacitance compare

to arteries. The structural plan of the wall is similar to that of other vessels, where the

amount of muscle is considerably less than in arteries. In most veins, especially in the

limbs, muscle is arranged circularly. Longitudinal muscle is present in iliac, portal,

renal veins and in superior and inferior vena cava. On the contrary, muscular tissue is

absent in placental veins, retinal veins; but these veins are consisting of endothelium

supported by variable amount of connective tissue. Pressure within the venous system

doesn’t exceed 5 mm of Hg. As the vein grows larger it decreases upto zero. Because

they contain small amount of muscle and usually vein have limited influence on blood

flow. (Fig. 1)

Due to any cause when there is sudden fall in blood pressure, there is reflex

constriction in vein to compensate the blood loss and tend to maintain the venous

return to the heart. Most veins have valves to prevent reflux of blood flow. When

blood flow reverses, if the semilunar valves cusps, not close properly, then blood fills

in expanded valve of the vein giving rise to knotted appearance to the distended vein.

Leg venous return is against gravity. Valves are of great importance. Blood is moved

towards the heart by intermittent pressures produced by contractions of the

surrounding muscles are absent in thorax and abdominal veins. 139

General Organization of Circulatory System :

Cells of the peripheral blood suspended in the plasma circulate throughout the

body in blood vascular system. Interstitial fluid from peripheral tissue returns to the

blood vascular system through the lymphatic system, which is preceding a channel for

migration of leucocytes and absorption of certain nutrients from the gut. The

cardiovascular system carries nutrients, oxygen, hormones throughout the body and

disperses heat. As a result of pulse pressure which is a mechanical difference between

systolic and diastolic pressure.

Blood circulates in a closed system where heart is the central pump, arteries

carry the blood to the peripheral part, veins returns to the heart. From the centre to the

periphery, arteries increase in number by repeated bifurcation. The valves of arteries

decrease in thickening towards periphery. Venules which return blood from periphery

progressively increase in size. Arteries are usually deeply situated than vein. Overall

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blood from the heart to all parts of the body carries through a series of tubes. Smooth

muscle is contractile where actin and myosin are organized in regular semilunar

manner. These tubes are composed of smooth muscles. Smooth muscles typically

found in tubular structure and hollow viscera, the actual arrangement of cells varies

with tissue. Smooth muscle has no attachment structure to the fasiae, tendons etc.

Blood supply of smooth muscle is extensive than striated muscles. 140

Composition of Vein : (Fig. 2)

Veins are composed of essentially three coats as that of arteries. But there are

variations in their relative thickness. If arteries are to be distinguished from veins

following reasons may be given

- The wall of a vein is very thin than the artery.

- The tunica media contains much collagen than arteries. The amounts of elastic

tissue are much less.

- In arteries tunica media, usually thicker than the adventitia. In contrast the

adventitia of veins is thicker than the media. In some large veins the adventitia

contains a considerable amount of elastic and muscle fibres which run in a

predominantly longitudinal direction. These fibres facilitate elongation and

shortening of the vena cava with respiration.

- A clear distinction between the tunica intima, media and adventitia cannot be

made out in small veins as all these layers consist predominantly of fibrous

tissue. Muscle is conspicuous by its complete absence in venous spaces of

erectile tissue, in veins of cancellous bone, dural venous sinuses, retinal veins

and placental veins. 141

Microscopic Structure of Vein :

(I) Tunica Intima - Endothelium

The endothelium is a mono-layer extending continuously over the entire

vascular tree. It is a key component of vessel wall playing major physiological roles.

Endothelial cells regulate diffusion of substances and migration of cells out of and

into the circulating blood, as these are in contact with blood stream, so influencing

blood flow. Ex : in the brain, endothelial cells of small vessels actively transport

substance like glucose into the brain parenchyma. In the process of ‘fibrinolysis’ or

clot dissolution by secreting a tissue plasminogen activator by endothelial cells, and

they have got phagocytic activity. Endothelial cells synthesize components of basal

lamina. They proliferate to provide new cells during growth in size of blood vessel to

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replace the damaged cells. Angiogenesis is stimulated by endothelial production in

response to locally low oxygen tension. It is important in wound healing and in

growth of tumors.

So overall, all the blood vessels including vein are lined with endothelial cells.

Cells are polygonal and elongated along the length of vessels. These endothelial cells

are sensitive to alteration in blood pressure, blood flow and oxygen tension in the

blood. They secrete various substances that can produce vasodilation by influencing

the tone of the muscles in vessel wall. They produce factors which controls the

coagulation of blood. Under normal condition clotting is inhibited, when required

clotting is facilitated. Under influence of adverse stimuli [ex : cytokines it has been

seen that T-lymphocytes produce cytokines and affect other cells. The function of the

cytokines is to stimulate the production of blood cells. Apart from T-cells cytokines

are also produced by monocytes, macrophages, endothelial cells. Some cytokines are

identified as interlukins, granulocytes stimulating factors, stem cell factor,

erythropoietin] endothelial cells undergo certain changes which facilitates passage of

lymphocytes through the vessel wall. Ex : in acute inflammation, endothelium allows

neutrophils to pass from blood into surrounding tissue. By influence of histamine

(stimulated by antigen mast cells release histamine into tissue) endothelium becomes

highly permeable allowing proteins and fluid to diffuse into the tissue resulting to

oedema. The changes that they occur in endothelium described above are taking place

very rapidly within fraction of minutes.

(II) Tunica Media :

It consists of concentric layers of circumferentially arranged smooth muscle

cells, with variable amount of elastin and collagen. Smooth muscle forms most of the

media of arteries and arterioles. A thin layer of smooth muscle also found in venules

and veins. Smooth muscle cells synthesize and secrete elastin and collagen which bear

directly on mechanical properties of vessels like distensibility cells support, elasticity,

rigidity. The muscle cells can be regarded as multifunctional mesenchymal cells.

After damaged to the endothelium, muscle cells migrate into the intima and

proliferate to reform the layer. In certain pathological conditions, muscles undergo

fatty degeneration, or participate in formation of atheromatous plaque.

(III) Tunica Adventitia :

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This layer is formed by general connective tissue varying in the thickness.

Vasa Vasorum :

Nourishment of tissue of vessel wall is provided by blood circulating vessels

itself. Large vessels have own vasculae supply within adventitia, in the form of

network of vessels called vasa vasorum. Vasa vasorum orginate from and and drains

into adjacent vessels which are peripheral branches. 142

Developmental Anatomy of Blood Vessels : 143 (Fig. 3)

The human yolksac has little yolk to nourish the developing embryo, blood

and blood vessel. Formation starts as early as 15-16 days in the mesoderm of the

yolksac, chorion, and body stalk. Blood vessels develop from isolated masses and

cords of mesenchyma in the mesoderm called blood islands. Spaces soon appear in

the islands and become the lumens of the blood vessels. Some of the mesenchymal

cells immediately around the spaces give rise to the endothelial lining of the blood

vessels. Mesenchyme around the endothelium forms the tunis of the larger blood

vessels. Growth and fusion of blood islands form an extensive network of blood

vessels throughout the embryo.

Development of Veins : The cardiovascular system is the first major system to function in the embryo.

The primordial heart and vascular system appear in the middle of the third week of

embryonic development. The heart starts to function at beginning of fourth week. This

precocious heart development is necessary because the rapidly growing embryo can

no longer satisfy it’s nutritional and oxygen requirement by diffusion alone.

Consequently, there is a need for an efficient method of acquiring oxygen and

nutrients from the maternal blood and disposing of carbon dioxide and waste

products.

Angiogenesis or blood vessel formation, begins in the extra-embryogenic

mesoderm of the yolksac, connecting stalk, and chorion. Embryonic blood vessels

begin to develop about two days later. The early formation of the cardiovascular

system is correlated with the absence of a significant amount of yolk in oocyte and

yolksac and the consequent urgent need for blood vessels to bring oxygen and

nourishment to the embryo from the maternal circulation through the placenta. At the

end of the second week, embryonic nutrition is obtained from the maternal blood by

diffusion through the extra embryonic coelom and yolksac. During the 3rd week and

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primordial uteroplacental circulation develops. Primordial blood vessels cannot be

distinguished structurally as arteries or veins, but are named according to their future

fates and relationship to the heart.

The formation of the embryonic vascular system involves two processes :

vasculogenesis and angiogenesis. Blood vessel formation in the embryo and

extraembryonic membranes during the 3rd week may be summarized as follows:

- Mesenchymal cells differentiate into endothelial cells precursor - angioblasts

(vessel-forming cells), which aggregate to form isolated angiogenic cell

clusters-blood islands.

- Small arteries appear within the blood islands by confluence of intercellular

clefts.

- Angioblasts flatten to form endothelial cells that arrange themselves around

the cavities in the blood island to form the endothelium.

- These endothelium lined cavities soon fuse to form networks of endothelial

channels. (vasculogenesis).

- Vessels sprout into adjacent areas by endothelial budding and fuse with other

vessels (angiogenesis).

Blood cells develop from the endothelial cells of vessels (hemangioblasts) as

they develop on the yolk sac and allantois at end of the third week. Blood formation

does not begin in the embryo until the 5th week. It occurs first in the various parts of

the embryonic mesenchyme, chiefly the liver and later in the spleen, bone marrow and

lymph nodes. Fetal and adult erythrocytes are derived from the different

hematopoietic progenitor cells. The mesenchymal cells surrounding the primordial

endothelial blood cells differentiate into the muscular and connective tissue elements

of the vessels. The earliest sign of the heart is appearance of pair endothelial strands -

angioblastic cords in the cardiogenic mesoderm during the 3rd week. These cords

canalize to form heart tubes, which fuse to form the tubular heart late in the 3rd week.

The heart begins to beat at 23rd day. An inductive influence from the anterior

endoderm stimulates early formation of the heart. The development of heart and blood

vessels is controlled by a cascade of regulatory genes and signaling molecules.

Three paired veins drain into the tubular heart of a four-week embryo -

- “Vitelline veins” return poorly oxygenated blood from the yolksac.

- “Umbilical veins” carry oxygenated blood from the primordial placenta.

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- “Common cardial veins” return poorly oxygenated blood from the body of the

embryo.

The vitelline veins follow the yolk stalk into the embryo. The yolk stalk is the

narrow tube connecting the yolksac with the midgut. After passing through the

septum transversum, the vitelline veins enter the venous end of the heart - the “sinus

venosus”. As the liver primordium grows into the septum transversum the hepatic

cords anastomose around pre-existing endothelium lined spaces. These spaces, the

primordial of the “hepatic sinusoids”, later become linked to the vitelline veins. The

“hepatic veins” form from the remains of the right vitelline vein in the region of the

developing liver.

The portal vein develops from an anastomosis network formed by the vitelline

veins around the duodenum.

The ‘umbilical veins’ run on each side of the liver and carry well oxygenated

blood from the placenta to the sinus venosus. As the liver develops, the umbilical

veins lose their connection with the heart and empty into liver. The right umbilical

vein disappears during the seventh week, leaving the left umbilical veins as the only

vessel carrying well-oxygenated blood from the placenta to the embryo.

Transformation of the umbilical veins may be summarized as follows ;

- The right umbilical vein and the caudal part of the left umbilical vein between

the liver and sinus venosus degenerate.

- The persistent caudal part of the left umbilical vein becomes the umbilical

vein, which carries all the blood from the placenta to embryo.

- A large venous shunt - the ductus venosus develops within the liver and

connects the umbilical vein with the inferior vena cava.

The cardinal veins constitute the main venous drainage system of the embryo.

The anterior and posterior cardinal veins drain cranial and caudal part of the embryo,

respectively. The anterior and posterior cardinal veins join the common cardinal

veins, which enter the sinus venosus. During the 8th week of embryonic development,

the anterior cardinal vein becomes connected by an anastomosis which shunts blood

from the left to the right anterior cardinal vein. This anastomotic shunt becomes the

left brachio-cephalic vein when caudal part of the left anterior cardinal vein

degenerates. The superior vena cava forms from the right anterior cardinal vein and

the right common cardinal vein.

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The posterior cardinal veins develop primarily as the vessels of the

mesocephalic (interim kidneys) and largely disappears with this transitory kidneys.

The only adult derivatives of the posterior cardinal veins are the root of the azygos

vein and the common iliac veins. The subcardinal and supracardinal veins gradually

replace and supplement the posterior cardinal veins. The sub-cardinal vein appears

first. They are connected with each other through the subcardinal anastomosis and

with the posterior cardinal veins through the nephric sinusoids. The sub-cardinal veins

form the stem of the left renal vein, the suprarenal veins, the gonadal veins and

segment of IVC. The supracardinal veins are the last pair of vessels to develop. They

become disrupted in the region of the kidneys. Cranial to this, they become united by

the an anastomosis i.e. represented in the adult by the azygos and hemi-azygos veins.

Caudal to the kidneys, the left supracardinal veins degenerates, but the right

supracardinal veins becomes the inferior part of the IVC.

Development of Superior Vena Cava : 144

The precardinal veins enlarge as the head and brain develop. They are further

augmented by the subclavian veins from the upper limb buds, and so become the chief

tributaries of the common cardinal veins, which gradually assume an almost vertical

position in association with the descent of the heart into the thorax. That part of the

original precardinal vein rostral to the subclavian is now the internaljugular vein, and

their confluence is the brachio-cephalic vein of each side. The right and left common

cardinal veins are originally of the same diameter. By the development of a large /

transverse connection, the left brachio-cephalic vein carries blood across from the left

to the right. The part of the original right precardinal vein between the junction of the

two brachio-cephalic and azygos veins forms the upper part of the superior vena cava,

the caudal part of the latter vessel is formed by the right common cardinal vein.

Caudal to the transverse branching of the left brachio-cephalic the left precardinal and

left common cardinal veins largely atrophy, the former constituting the terminal part

of the left superior intercostal vein; while the latter is represented by the ligament of

the left vena cava and the oblique vein of the left atrium. The remainder of the left

superior intercostal is developed from the cranial end of the post cardinal vein and

drains the second, third, on occasion the fourth intercostal veins. The oblique vein

passes downwards across the back of the left atrium to open into the coronary sinus

which, as already indicated, represents the persistent left horn of the sinus venosus.

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67

Right and left superior venae cavae are present in some animal and occasionally in

mankind.

Development of Inferior Vena Cava :

The inferior vena cava (IVC) forms during a series of changes in the

primordial veins of the trunk that occur as blood, returning from the caudal part of the

embryo, is shifted from the left to the right side of the body. The IVC is composed of

four main segments

- A hepatic segment derived from the hepatic vein (proximal part of right

vitelline vein) and hepatic sinusoids.

- A prerenal segment derived from the right subcardinal vein.

- A renal segment derived from the subcardinal-supracardinal anastomosis.

- A postrenal segment derived from the right supracardinal vein.

The early postcardinal veins communicate across the midline via an inter-post-

cardinal anastomosis between the iliac veins, and become the major part of the

definitive left common iliac vein. It diverts an increasing volume of blood into the

right longitudinal veins, which accounts for the ultimate disappearance of the most of

those on the left.

The supracardinal veins receive the larger venous drainage of the growing

body wall. The right supracardinal vein persists and forms the greater part of the post

renal segment of the IVC. The continuity of the vessel is maintained by the

persistence of the anastomosis of between the right supracardinal and right

subcardinal vein in the renal collar.

In summary, therefore, the inferior vena cava is formed from below upwards

by the confluence of common iliac veins; short segment of the right postcardinal vein,

the postcardinal-supracardinal anastomosis, part of the right supra-cardinal vein, a

new anastomotic channel of double origin, the hepatic segment of the inferior vena

cava; and the cardiac termination of the right vitelline hepatocardiac vein.

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Physiology of Veins

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2. PHYSIOLOGY OF VEINS

Usually physiology explains the physical and chemical factors that are

responsible for the origin, development and progression of life. The human

physiology is concerned, we are concerned with specific characteristics and

mechanisms of the human body, that make it a living being.

The basic unit of the body is cell. Each type of cell is specially adopted to

perform functions. About sixty percent of the adult human body fluid inside the cell is

called intra-cellular fluid. About one third is in space outside the cell is called

extracellular fluid. This extracellular fluid is in constant motion throughout the body.

It is rapidly transported in circulating blood and mixed between blood and tissue fluid

by diffusion. In extracellular fluid nutrients needed by the cells for maintenance of the

their life. Extracellular fluid is called internal environment of the body. The

extracellular fluid cells those are capable of living, growing, performing need proper

concentration of o2, glucose, ions, amino acids, fatty acids and other nutrients.

Extracellular fluid contains sodium, chloride, bicarbonate, oxygen, glucose, fatty

acids, amino acids. It also contains carbon dioxide, which is transported from cells to

the lungs. The intracellular fluid differs completely. It contains Potassium, phosphate,

Magnesium etc.

Homeostasis: 145

The term homeostasis is maintenance of constant internal environment so that

all the tissues of the body perform their function to maintain constant conditions;

where lungs provide oxygen to the extracellular fluid, kidneys, maintain ion

concentration, GIT provides nutrition. So collectively all together is homeostasis.

Usually extracellular fluid is transported through all parts of body in two stages : one

is movement of blood in and around circulatory system, movement of fluid between

the capillaries and cells [Guyton Fig. 1.1].

As the blood passes through the capillaries there is continuous exchange of

extracellular fluid, that occurs between plasma of portion of blood and interstitial

fluid, which fills intercellular spaces [Fig. 1.2] Note that capillaries are porous, so that

large amount of fluid and its dissolved constituents can diffuse back between blood

and tissue spaces. This process of diffusion is caused by kinetic motion of molecules

in both plasma and interstitial fluid.

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69

Thus the extracellular fluid is continuingly being mixed, there by maintaining

almost homeostasis of the body. When blood passes throughout the body, it passes

through lungs also, blood picks up oxygen in alveoli needed by cells. The oxygen

diffuses by molecular motion through this membrane into the blood. In the same way

water and ions diffuse through tissue capillaries. A large portion of blood pumped by

the heart passes through the walls of the GI tract organs where different dissolved

nutrients are absorbed from the ingested food into the extracellular fluid. All the

substances absorbed from GIT not utilized from the cells. The liver changes the

chemical composition of these substances to more usable from to all tissues. At the

sometime blood picks up o2 from the lungs, CO2 released blood into alveoli, so that

the co2 is most abundant end product of metabolism. Passage of blood through

kidneys removes most of the substances like CO2, urea, uric acid, excess ions and

water. The human body is literally thousands of control systems in it. But the most of

significant of these is genetic controlled system. Many others control system operate

by nervous and humoural regulations (chemical).

Oxygen is one the major substance required for the chemical reactions in the

cells. It is god gift that body has special control mechanism to maintain exact constant

o2 concentration in the extracellular fluid. It is principally depending on chemically

characteristics of hemoglobin present in RBCs. Hemoglobin combines with o2 as

blood passes through the lungs. Then blood passes through the capillaries. Because of

its strong chemical affinity, it doesn’t release the oxygen to tissue fluid, if too much

oxygen is already there. If oxygen concentration is too low there sufficient oxygen is

released for adequate oxygen concentration. Like this carbon dioxide concentration in

the extracellular fluid is also essential. This is end product of the oxidative reaction in

cells. If all carbon dioxide formed in the cells accumulate in tissue fluids, exciting

respiratory centres causing to breath deeply and rapidly. So several systems like baro-

receptor systems, and chemical receptor systems are responsible for it.

An Overview of Circulation: 146 [Fig. 4 (a)]

The function of circulation is to serve the needs of the tissue such as nutrients,

o2, hormones and also to transport waste products away, in general to maintain an

appropriate environment in all the tissue fluids for survival and function of the cells.

Sometimes it is difficult to understand how blood flow is controlled according to

tissue needs.

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The circulation is divided into (1) systemic circulation and (2) pulmonary

circulation. Systemic circulation supplies all the tissues of the body except the lungs

with blood flow, it is called peripheral circulation. The vascular system in each

separate tissue of the body has its own special characteristics, some general principles

of vascular system apply in all the parts of the body. The function of arteries is to

transport blood under high pressure to the tissues. As arteries have strong vascular

walls, so blood flows rapidly in arteries. The arterioles are the last small branches of

the arterioles system and they act as control valves through which blood is released

into the capillaries. The arteriole has the strong muscular wall, capable of closing and

dilating, having capability of vastly altering blood flow to the capillaries in response

to the need of the tissues. The function of the capillaries is to exchange the fluid

nutrients, fluids, electrolytes, hormones and other substances between the blood and

interstitial fluid. For this purpose the capillary walls are very thin and permeable to

small molecule substances. The venules collect blood from the capillaries, which

gradually coalesce into progressive larger veins. The veins function as conduits for

transport of blood from tissues back to the heart and serve as the major reservoir of

the blood, because the pressure in venous system is very low. The venous walls are

thin. Depending upon the needs of the body they also contract and expound.

Volumes of Blood in Different parts of Body : [Fig.4(b)]

64 % in veins, 13% in arteries, 7% in arterioles and capillaries, 7 % in heart

and 9 % in pulmonary vessels.

Cross Sectional Areas of the Blood Flow :

Aorta 2.5 cm2

Small Arteries 20 cm2

Arteries 40 cm2

Capillaries 2500 cm2

Venuoles 250 cm2

Small veins 80 cm2

Venae cavae 8 cm2

Crosssectional areas of vein are much larger than the arteries which explains

large storage of blood in venous system. The same volume of blood flows through

each segment of circulation each minute. The velocity of blood flow is inversely

proportional to its crossectional area.

Basic Theory of Circulatory Function :

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71

When tissues are active, they need more blood flow. Heart normally cannot

increase its cardiac output more than 4-7 times. Therefore, it is not possible to

increase blood flow everywhere in the body. When a particular tissue demands

increased flow. Instead, micro-vessel of each tissue are monitoring the tissue needs,

such as availability of oxygen and other nutrients and the accumulation of waste

products. And these in turn control local blood flow to the level of tissue need. The

cardiac output is controlled mainly by the sum of all local tissue flows. When blood

flows through a tissue it immediately returns by the way of veins to the heart. The

heart responds to this increased inflow by pumping all the blood immediately back to

the arteries.

Vascular Distensibility: 147

The valuable characteristic of blood vessels is that they are distensible. Ex :

when a pressure in arterioles is increased this dilates, the arterioles. Therefore,

decreases their resistance. The result is increased blood flow, not only because of

increased pressure, but also because of decreased resistance.

The distensibility of arteries and veins are different. Anatomically the walls of

arteries are far stronger than those of veins. Consequently, veins are eight times

distensible as the arteries. That means, a given in rise of pressure causes about eight

times much extra blood to fill a vein as to fill an artery.

Effect of Sympathetic Stimulation or Inhibition on Blood Vessels :

Large changes are observed in blood flow caused by increased or decreased

sympathetic stimulation. Because inhibition of sympathetic stimulation greatly dilate

the vessels and can increase the blood flow. Conversely, strong sympathetic

stimulation can constrict the vessels so much that blood flow can be decreased as low

as zero.

Regarding volume, pressure, relations are concerned, sympathetic stimulation

increases vascular smooth muscle tone, where it increases pressure at each volume of

arteries or veins; where as sympathetic inhibition decreases the pressure at each

volume. For an instance, increase in vascular tone throughout systemic circulation

often causes large volume of blood to shift into the heart, which is a reason for

increased heart pumping, sympathetic controls of vascular capacity is especially

important during loss of blood [hemorrhage]. Enhancement of sympathetic tone of

vessels, especially of veins reduces, the vessel sizes, so that the circulation continues

to operate almost normally even when 25% of total blood volume has been lost.

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Veins and their Functions: 148

For years, the veins have been considered to be nothing more than passage

ways, for flow of blood into the heart. But it is becoming apparent that they perform

many special functions that are necessary to the operation of circulation. They are

capable of constricting and enlarging, there by storing small or large quantity of blood

and making this blood available when it is required by the circulation. Vein can also

propel blood forward by means of which called venous pump, which will regulate

even cardiac output.

To understand various functions of vein is necessary to know the pressures in

the vein and how they are regulated. Blood from all systemic veins flows into right

atrium so the pressure in the right atrium is called central venous pressure. Anything

that affects right atrial pressure definitely affect venous pressure everywhere in the

body. Right atrial pressure is regulated by balance between the ability of the heart to

pump blood out of the right atrium and tendency for blood to flow from the peripheral

vessels back into the right atrium. The normal right atrial pressure is about zero mm

of Hg which is equal to the atmospheric pressure of the body. It can rise to 20-30 mm

of Hg under abnormal condition, where there is serious heart failure and massive

transmission of blood.

Large veins have little resistance to the blood flow, when they are distended.

The large veins usually offer considerable resistance to the blood flow, because of this

the pressure in the peripheral veins is 4-7 mm of Hg. that is greater than the right

atrial pressure. This central pressure is regulated by right atrial pressure, peripheral

venous pressure, pressure of abdominal vein and venous pressure of the leg.

Effect of Hydrostatic Pressure on Volume Pressure :

In any body of water, the pressure at the surface of the water is equal to

atmospheric pressure, but the pressure rises one mm of Hg for each 13.6 mm distance

below the surface. This pressure results from the weight of the water and therefore is

called hydrostatic pressure. Hydrostatic pressure also occurs in the vascular system of

the human being because of the receipt of the blood in the vessels, when a person is

standing, the pressure in the right atrium remains about ‘0’ mm of Hg because the

heart pumps into the arteries any excess blood that attempts to accumulate at this

point. However, in an adult who is standing absolutely still, the pressure in the veins

of the feet is about + 90 mm of Hg. Simply because of the hydrostatic weight of the

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Physiology of Veins

73

blood in the veins between the heart and the feet. The venous pressures at other levels

of the body to proportionately between zero and 90 mm of Hg.

In the arm veins, the pressure at the level of the top rib is usually about + 6

mm of Hg, because of compression of the subclavian vein as it passes over the this

rib. The hydrostatic pressure down the length of the arm is then determined by the

distance below the level of this rib. Thus, if the hydrostatic difference between the

level of the rib and the hand is 29 mm of Hg. This hydrostatic pressure is added to the

6 mm of Hg pressure caused by compression of the vein as it crosses the rib, making a

total of 35 mm of Hg pressure in the veins of the hand.

The neck veins of an upright person collapse almost completely all the way to

the skull owing to atmospheric pressure on the outside of the neck. This collapse

causes the pressure in these veins to remain zero along their entire extent. The reason

for this is that any tendency for the pressure to rise above this level opens the veins

and allows the pressure to fall back to zero because of increased flow of the blood. On

the other hand, any tendency for the pressure to fall below this level collapses the

veins still more, which increases their resistance and again returns the pressure back

to zero.

The veins inside the skull, however, are in a non-collapsible chamber and they

will not collapse consequently, negative pressure can exist in the dural sinuses of

head, in the standing position, the venous pressure in the sagital sinus is about – 10

mm of Hg, because of the hydrostatic “suction” between the top of the skull and the

base of the skull. Therefore, if the sagital sinus is opened during surgery, air can be

sucked immediately into this vein; the air may even pass downward to cause air

embolism in the heart, so that the heart valves will not function satisfactorily, and

death can ensue.

Venous Valves and the “Venous Pump” their Effects on Venous Pressure:

Were it not for valves in the veins, the hydrostatic pressure effect would cause

the venous pressure in the feet always to be about + 90 mm of Hg in standing adult.

However, every time one moves the legs, one tightens the muscles and compresses

the veins either in the muscles or adjacent to them, and this squeeze the blood out of

the veins. The valves in the veins, are arranged so that the direction of blood flow can

be only toward the heart. Consequently, every time a person moves the legs or even

tenses the muscles, a certain amount of blood is propelled toward the heart and the

pressure in the veins is lowered. This pumping system is known as the “venous pump:

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74

or the “muscle pump”, and it is efficient enough that under ordinary circumstances,

the venous pressure in the feet of a walking adult remains close to or less than 25 mm

of Hg.

If a human being stands perfectly still, the venous pump doesn’t work, and the

venous pressures in the lower part of the leg will rise to the full hydrostatic value of

90 mm of Hg in about in 30 seconds. The pressure in the capillaries also increase

greatly causing fluid to leak from the circulatory system into the tissue spaces. As a

result, the legs swell, and the blood volume diminishes, indeed, 10-20 % of the blood

volume can be lost from the circulatory system within the first 15 minutes of standing

absolutely still, as often occurs when a soldier is made to stand at attention.

Venous Pressure Incompetence and Varicose Veins :

The valves of the venous system frequently become “incompetent” or

sometimes are even destroyed. This is especially true when the veins have been

overstretched by excess venous pressure lasting weeks or months, as occurs in

pregnancy or when one stands most of the time. Stretching the veins increases their

cross-sectional areas, but the leaflets of the valves no longer close completely. When

this develops, the pressures in the veins of the legs increases still more owing to

failure of venous pump; this further increases the size of the veins and finally destroys

the function of the valves entirely. Thus the person develops “varicose veins”, which

are characterized by large bulbous protrusions of the veins beneath the skin of the

entire leg and particularly the lower leg. The venous and capillaries cause constant

edema in the legs whenever these people stand for more than a few minutes. The

edema inturn prevents adequate diffusion of nutritional materials from the capillaries

to the muscle and skin cells, so that the muscles become painful and weak the skin

frequently becomes gangrenous and ulcerates. The best treatment for such a condition

is continual elevation of the legs to a level at least as high as the heart, but tight

binders on the legs are also of considerable aid in preventing the edema and its

sequelae.

Blood Reservoir and Function of Vein :

Venous system serves as blood reservoir for the circulation when blood is lost

from the body and arterial pressure begins to fall, pressure reflexes are elicited from

carotid sinuses and other pressure sensitive areas of circulation. These inturn send

sympathetic nerve signals to the veins causing them to constrict. So even after as

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much as 20 % of total blood volume has been lost. The circulatory system often

functions almost normally because of reservoir function of veins.

Specific Blood Reservoirs :

Certain portions of circulatory system are extended to some other portions

called blood reservoirs. These include spleen, liver, large abdominal veins, venous

plexus, beneath the skin altogether contribute more than thousand ml of blood.

The Spleen as a Reservoir for Storing Red Blood Cells : [Fig. 4 (c)]

The spleen has two separate areas for storing blood; the venous sinuses and

pulp. Small vessels flow directly into the venous sinuses, and the sinuses can swell the

same as any other part of the venous system and store whole blood. In the splenic

pulp, the capillaries are so permeable that whole blood oozes through the capillary

walls into a trabeculae mesh forming the red pulp. The red cells are trapped by the

trabeculae, where as the plasma returns into the venous sinuses and then into general

circulation. As a consequence, the red pulp of the spleen is as special reservoir of

extra red blood cells that are expelled into the general circulation when the

sympathetic nervous system is excited and contracts the spleen or its vessels. In the

lower animals, this extra-storage of red blood cells is much greater than in humas, but

in even in the human, possibly much as 50 millions of concentrated red blood cells

can be released into the circulation, raising the hematocrit 1-2 %.

In other areas of the splenic pulp are islands of white blood cells, which

collectively are called the white pulp. Here lymphoid cells are manufactured similar

to those manufactured in the lymph nodes. They are part of the body’s immune

system. Blood Cleansing Function of the Spleen - Removal of Old Cells :

Blood passing through the splenic pulp before it enters the sinuses undergoes

thorough squeezing. Therefore, it is to be expected that fragile red blood cells would

not withstand the trauma. For this reason, many of the red blood cells destroyed in the

body have their final demise in the spleen. After the cells rupture, the released

hemoglobin and the cells stroma are ingested by the reticuloendothelial cells of the

spleen.

Reticuloendothelial Cells of the Spleen :

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The pulp of the spleen contains many large phagocyte reticuloendothelial cells

and the venous sinuses are lined with similar cells. These cells act as a cleansing

system for the blood, acting in concert with a similar system in the venous sinuses of

the liver. When the blood is invaded by infectious agents, the reticuloendothelial cells

of the spleen rapidly remove debris, bacteria, parasites, and so forth. Also, in many

infectious processes, the spleen enlarges in the same manner the lymph glands enlarge

and then erforms its cleansing function even more adequately.

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Microcirculation

77

3. MICROCIRCULATION

The most purposeful function of the circulation occurs by the transport of

nutrients to the tissues and removal of cellular excreta. The small arterioles control the

blood flow to each tissue area. The most instances controls its own blood flow its

relation to its needs.

The capillaries are extremely thin structures with walls of a single layer of

highly permeable endothelial cells. Here interchange of nutrients of cellular excrita

occurs between the tissues and circulating blood. about 10 billion capillary with a

total surface area estimated to be 500-700 mm of sq mt. It is very essential to know

the factors that they affect the transfer of fluid through capillary walls between

circulating blood and interstitial fluid.

Anatomy of Microcirculation149 :

The microcirculation of each part of the body is specifically serve special

needs of that part. In general arteries become small enough to be called arterioles,

which generally have internal diameter less than 20 micrometers. The

microcirculation of each organ specifically organize to serve organ special needs. As

arteries become small enough to become arteries then blood enters from arteriole to

capillaries and leaves by the way of venule, the venules are considerably larger than

the arterioles and have a much weak muscular coat. Blood causally doesn’t flow

continuously through the capillaries. Instead it flows intermittently turning on and off

every few seconds. The most important factor found thus far to affect he degree of

opening closing off meta arterioles and pre-capillaries sphincter (Fig 16.2) is the

concentration of oxygen in tissues. When the rate of oxygen use is great the

intermittent periods of blood flow occur more often there by allowing the blood by

carrying increased qualities of oxygen to the tissues.

There is an average rate of blood flow through tissue capillary bed and an

average rate of transfer of substances between the blood of the capillaries and the

surrounding interstitial fluid. Billions of individuals capillaries are responding to the

local condition to the tissue.

Exchange of Nutrients Blood and Interstitial Fluid :

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Microcirculation

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Diffusion through the capillary membrane : [Fig. 4 (d)]

Substance are transferred between plasma and interstitial fluid is by diffusion.

Blood transverses the capillary, tremendous number of water molecules and dissolved

particles move through the capillary wall. Diffusion results from thermal motion of

water molecules and dissolved substances in the fluid. Different particles moving first

into one direction and then in another direction.

Lipid soluble substances can diffuse directly through the cell walls of capillary

endothelium. If a substance is lipid soluble it can diffuse directly through the cell

membrane of capillary without having to go through the pores. The substances

include oxygen carbon dioxide as great as the rate at which plasma itself flows

linearly along the capillary. That is, the water of the plasma is exchanged with water

of the interstitial fluid 80 times before the plasma can go the entire distance through

the capillary.

Effect of Molecular Size of Passage through Pores :

The width of capillary intercellular cleft-pores, 6-7 nanometer, is about 20

times the diameter of the water molecule, which is the smallest molecule that

normally pass through the capillary pores. On the other hand, the diameters of plasma

protein molecules are slightly greater than the width of the pores. Other substances

such as sodium ions, chloride ions, glucose, and urea, have intermediate diameters.

Therefore, the permeability of the capillary pores for different substances varies

according to their molecular diameters.

The capillaries in different tissues have extreme differences in their

permeabilities. For instance, the membrane of the liver capillary sinusoids is so

permeable that even plasma proteins pass freely through these walls almost as easily

as water and other substances. Theses substances can permeate all areas of the

capillary membrane, the rate of transport through the capillary membrane are many

times the rates for most lipid-insoluble substances such as sodium ions and glucose.

Water-Soluble Substances Diffuse Only through Intercellular “Pores” in the

Capillary Membrane :

Many substances needed by the tissues are soluble in water but cannot pass

through the lipid membranes of the endothelial cells, such substances include water

molecules themselves, sodium ions, chloride ions, and glucose. Despite the fact that

not more than 1/1000 of the surface area of the capillaries are represented by the

intercellular cleft between the endothelial cells, the velocity of thermal molecular

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motion in the cleft is so great that even this small area is sufficient to allow

tremendous diffusion of water and water soluble substances through these cleft-pores.

To give one an idea of the rapidity with which these substances diffuse, the rate at

which water molecules diffuse through the capillary membrane is about 80 times.

Also the permeability of the renal glomerulae and muscle permeabilities for protein

are about the same. The degrees of capillary permeability are greater in liver, for

instance, to transfer tremendous amounts of nutrients between the blood and the liver

parenchymal cells and the kidneys to allow filtration of large quantities of fluid for the

formation of urine.

Effect of Concentration of Difference on Net Rate of Diffusion through the

Capillary Membrane :

The ‘net’ rate of diffusion of a substance through any membrane is

proportional to the concentration difference between the two sides of the membrane.

That is, the greater the difference between the concentrations of any given substance

on the two sides of the capillary membrane, the greater will be the net movement of

the substance in one direction through the membrane. Thus, the concentration of

oxygen in the blood is normally greater than that in the interstitial fluid. Therefore,

large quantities of oxygen normally move from the blood toward the tissues.

Conversely, the concentration of carbon dioxide is greater in the tissues than in the

blood which causes carbon dioxide to move into the blood and to be carried away

from the tissues.

The rates of diffusion through the capillary membranes of most nutritionally

important substances are so great that only slight concentration differences suffice to

cause more than adequate transport between the plasma and interstitial fluid. For

instance, the concentration of oxygen in the interstitial fluid immediately outside the

capillary is probably no more than 1 % less than the concentration in the plasma of

blood, and yet this 1 % difference causes enough oxygen to move from the blood into

the interstitial spaces to provide all the oxygen required for tissue metabolism.

The Proteins in the Plasma and Interstitial Fluid mainly Determine the Plasma and

Interstitial Fluid Volume :

The pressure in the capillaries tends to force fluid and its dissolved substances

through the capillary pores into the interstitial spaces. In contrast, osmotic pressure

caused by the plasma protein tends to cause fluid movement by osmosis from the

interstitial spaces into the blood, this osmotic pressure prevents significant loss of

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fluid volume from the blood into the interstitial spaces. Also important is the

lymphatic system, which returns back to the circulation the small amounts of protein

that do leak into the interstitial spaces.

The Interstitium and Interstitial Fluid :

The about one sixth of the body consists of spaces between cells, which

collectively are called the interstitium. The fluid in these spaces is the interstitial fluid.

The structure of the interstitium has two major type of solid structures :

(1) Collagen fibre bundles and proteoglycan filaments. The collagen fiber

bundles extend long distances in the interstitium. They area extremely strong

and therefore provide most of the tensional strength of the tissues. The

proteoglycan filaments, on the other hand, are extremely thin, coiled

molecules composed by about 98 % hyaluronic acid and 2 % protein. These

molecules are so thin that they can never be seen with a light microscope and

are difficult to demonstrate even with the electronic microscope. Nevertheless,

they form a mat of very fine reticular filaments aptly described as “brush pile”.

(2) ‘Gel’ in the Interstitium - the fluid in the interstitium is derived by filtration

and diffusion from the capillaries. It contains the almost same constituents as

plasma except for much lower concentration of proteins. As proteins don’t

pass the walls of capillaries with ease. The interstitial fluid is mainly entaped

in the minutes spaces among the proteoglycan filaments and the fluid present

within them has characteristics of ‘get’. Therefore, called as tissue gel.

Because of the large number of proteoglycan filaments, it is difficult for fluid

to flow through tissue ‘gel’, but still then it diffuses through the gel only diffusion

through cell occurs 99 % rapidly rather than free fluid. So the diffusion allows rapid

transport of electrolyte nutrients, oxygen, carbon dioxide and cellular excreta.

Interstitial Pressure :

As the body is surrounded by tight encasement, such as cranial vault around

the brain, strong fibrous capsule around the kidney, fibrous sheaths around the

muscles, sclera around the eye, the interstitial fluid pressure is positive in these areas.

One should remember that pressure exerted on skin is atmospheric pressure and

normal interstitial fluid pressure is usually negative, as per previously heard concept,

interstitial fluid pressure is always positive. There is general belief that true interstitial

fluid pressure in the tissues is slightly less than atmospheric pressure.

Lymphatic system is the basic cause of negative pressure :

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Lymphatic system plays its role in determining interstitial fluid pressure.

Lymphatic system is scavenger, which removes the excess of fluid, protein, debris etc

and other matter from the tissue spaces. When fluid enters the lymphatic capillaries,

any movement of the tissue propels the lymph forward through the lymphatic system,

eventually emptying back into the circulation. In this way, any time any free fluid

accumulates in the tissue, it is simply pumped away as a consequence of tissue

movement, when the amount of fluid leaking from the blood capillaries is slight, as it

true for most tissues, research evidence suggests that actually pump a slight

intermittent negative pressure that gives an average negatively in the loose tissue.

“Plasma Colloid Osmotic Pressure” - Proteins in the Plasma Cause Colloid

Osmotic Pressure :

The proteins are the only dissolved substances in the plasma and interstitial

fluid, much of these are soon removed from the interstitial spaces by way of the

lymph vessels. Therefore, the concentration of protein in the plasma averages about

three times as much as that in most interstitial fluid; 7.3 gm/dl in the plasma versus 2-

3 gm/dl in the interstitial fluid. Only those molecules or ions that fail to pass through

the pores of semi-permeable membrane exert osmotic pressure. Because the proteins

are the only dissolved constituents that do not readily penetrate the pores of the

capillary membrane. It is the dissolved proteins of the plasma and interstitial fluids

that are responsible for the osmotic pressure at the capillary membrane. To distinguish

this osmotic pressure from that which occurs at he cell membrane, it is called either

colloid osmotic pressure or oncotic pressure. The term “colloid” osmotic pressure is

derived from the fact that a protein solution resembles a colloidal solution despite the

fact that it is actually a true molecular solution.

Exchange of Fluid volume through the Capillary Membrane :

Now that the different factors affecting fluid movement through the capillary

membrane have been discussed, the average capillary pressure at the arterial ends of

the capillaries is 15-25 mm of Hg greater than at the venous ends. Because of this

difference, fluid “filters” out of the capillaries at their arterial ends, and at their

venous ends, fluid is reabsorbed back into the capillaries. Thus a small amount of

fluid actually “flows” through the tissues from the arterial ends of the capillaries to

the venous ends. The dynamics of this flow are as follows :

Analysis of the Forces Causing Filtration at the Arterial End of the Capillary:

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The approximate average forces operative at the arterial end of the capillary

that cause movement through the capillary membrane are shown as follow:

TABLE NO. 13 SHOWING ANALYSIS OF FORCES AT ARTERIAL END OF CAPILLARY

Factors mm of Hg

Forces tending to move fluid outward capillary pressure 30

Negative interstitial fluid pressure 03

Interstitial fluid colloid osmotic pressure 08

Total Outward Force = 41

Forces tending to move fluid inward :

Plasma colloid osmotic pressure 28

Total inward force 28

Summation of Force

Outward 41

Inward 28

Net Outward Force 13

Thus the summation of the forces at the arterial end of the capillary shows a

net filtration pressure of 13 mm of Hg, tending to move fluid in the outward direction.

This 13 mm of Hg filtration pressure causes, on the average, about 0.5 % of the

plasma in the flowing blood to filter out of the arterial end of the capillaries into the

interstitial spaces.

Analysis of Re-absorption at the Venous End of the Capillary : [Fig. 2 (c)]

The low pressure at the venous end of the capillary changes the balance of

forces in favour of absorption. The force that causes the fluid to move into the

capillary , 28 mm of Hg, is greater than that opposing reabsorption, 21 mm of Hg. the

difference, 7 mm of Hg, is the reabsorption pressure at the venous ends of the

capillaries. This reabsorption pressure is considerably less than the filtration pressure,

but remember that the venous capillaries are more numerous and more permeable than

the arterial capillaries, so that less pressure is required to cause the inward movement

of fluid.

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The reabsorption pressure causes about nine tenth of the fluid that has filtered

out of the arterial ends of the capillaries to be reabsorbed at the venous ends. The

remainder flows into the lymph vessels. Under normal conditions, a state of near

equilibrium exists at the capillary membrane, where by the amount of fluid filtering

outward from some capillaries equals almost exactly the quantity of fluid that is

returned to the circulation by absorption through other capillaries. The slight

disequilibrium that does occur account for the small of fluid that is eventually

returned by way of the lymphatics.

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4. LYMPHATIC SYSTEM

The lymphatic system149 represents an accessory route by which fluid can flow

from the interstitial spaces into the blood. And, most important the lymphatics can

carry the proteins and large particulate matter away from the tissue spaces, neither f

which can be removed by absorption directly into the blood capillary. This removal of

proteins from the interstitial spaces is an essential function, without which we would

die within about 24 hours. The lymphatic system consists of fluid called “LYMPH”.

The vessels called “Lymphatic Vessels” to transport the fluid.

Lymph Channels of the body :

Almost all the tissues of the body have lymphatic channels that drain excess

fluid directly from the interstitial spaces. The exceptions include the superficial

portions of the skin, the central nervous system, deeper portions of peripheral nerves,

the endomysium of muscles, and the bones. Even these tissues have minute interstitial

channels called prelymphatics through which interstitial fluid can flow; this fluid

eventually flows either into lymphatic vessels, in the case of the brain, into the

cerebrospinal fluid and directly back into the blood.

Essentially all the lymph from the lower part of the body flows up the thoracic

duct and empties into the venous system at the junction of the left internal jugular

vein and subclavian vein. Lymph from the left side of the head, the left arm, and parts

of the chest region also enters the thoracic duct before it empties into the veins.

Lymph from the right side of the neck and head, the right arm, and parts of thorax

enters the right lymph duct, which then empties into the venous system at the junction

of the right subclavian vein and internal jugular vein.

Terminal Lymphatic Capillaries And Their Permeability: [Fig. 5 (b) & (d)]

Most of the fluid filtering the arterial capillaries flows among the cells and is

finally reabsorbed back into the venous ends of the blood capillaries. But on the

average probably about one tenth of the fluid enters the lymphatic capillaries instead

and returns to the blood through the venous capillaries. The total quantity of this

lymph is normally only 2-3 liters each day.

The minute quantity of fluid that returns into the circulation by way of the

lymphatics is extremely important because substances of high molecular weight, such

as proteins, cannot be reabsorbed in any other way. Yet they can enter the lymphatic

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capillaries almost unimpeded. The reason for this is a special substance of the

lymphatic capillaries. The endothelial cells of the capillaries attached by anchoring

the filaments to the surrounding connective tissue. At the junctions of the adjacent

endothelial cells, the edge of the adjacent cell in such a way that the overlapping edge

is free to flap inward, thus forming a minute valve that opens to the interior of the

capillary. Interstitial fluid, along with its suspended particles, can push the valve open

and flow directly into the lymphatic capillary. But this fluid has difficulty leaving the

capillary once it has entered because any backflow will close the flap valve. Thus the

lymphatics have valves at the very tips of the terminal lymphatic capillaries as well as

valves along their larger vessels upto the point where they empty into the blood

circulation.

Formation of Lymph :

Lymph is derived from interstitial fluid that flows into the lymphatics.

Therefore, lymph as it first flows from each tissue has almost the same composition as

the interstitial fluid. The position concentration in the interstitial fluid of most tissues

averages about 2 gm/dl, and the protein concentration of lymph flowing from these

tissues is near this valve. On the other hand, lymph formed in the liver has a protein

concentration as high as 6 gm/dl and lymph formed in the intestines has a protein

concentration as high as 3-4 gm/dl because about two thirds of all lymph normally is

derived from the liver and intestines, the thoracic lymph, which s a mixture of lymph

from all areas of the body, usually has a protein concentration of 3-5 gm/dl. The

lymphatic system is also one of the major routes of nutrients from the gastrointestinal

tract, being responsible principally for the absorption of fats. Indeed, after a fatty

meal, thoracic duct lymph sometimes contains as much as 1-2 % fat. Finally, when

large particles, such as bacteria, can push their way between the endothelial cells of

lymphatic capillaries and in this way enter the lymph. As the lymph passes through

the lymph nodes, these particles are removed and destroyed.

Rate of Lymph Flow :

About 100 ml of lymph flows through the thoracic duct of a resting human per

hour, and perhaps another 20 ml flows into the circulation each hour through other

channels, making a total estimated lymph flow of about 120 ml/hr between 2 and 3

lts/day.

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Effect of Interstitial Fluid Pressure on Lymph Flow : [Fig. 5 (c)]

The lymph is slight at interstitial fluid pressures more negative than -6mm Hg.

Then, as the pressure rises upto valves slightly greater than 0 mm Hg the flow

increases more than 20 fold. Therefore, any factor that increases interstitial fluid

pressure will normally also increase the lymph flow such factors include the following

Elevated capillary pressure

Decreased plasma colloid osmotic pressure

Increased interstitial fluid protein

Increased permeability of the capillaries.

All of these cause the balance of fluid exchange at the blood capillaries

membrane to favor fluid movement into the interstitium, thus increasing interstitial

fluid volume, interstitial fluid pressure and lymph flow all at the same time. However,

note that when the interstitial fluid pressure becomes 1-2 millimeter greater than

atmospheric pressure (0 mm Hg), lymph flow fails to rise further at still higher

pressures. This probable result from the fact that increasing tissue pressure not only

increases entry of fluid into lymphatic capillaries, but also compresses the outside

surfaces of the larger lymphatics, thus impeding lymph flow. At these higher

pressures, these two factors appear to balance each other almost exactly.

Like veins, lymphatic vessels contain valves, which ensure the one-way

movement of lymph. Ultimately, lymph drains into venous blood through the right

lymphatic junction of the internal jugular and subclavian veins. Thus, the sequence of

fluid flow is blood capillaries interstitial spaces lymphatic capillaries (lymph)

lymphatic vessels lymphatic ducts subclavian veins.

The same two “pumps” that aid return of venous blood to the heart maintain

the flow of lymph.

(1) Skeletal Muscle Pump : The “milking action” of skeletal muscle contractions

compresses lymphatic vessels and forces lymph toward the subclavian veins.

(2) Respiratory Pump : Lymph flow is also maintained by pressure changes that

occur during inhalation. Lymph flows from the abdominal region, where the

pressure is higher, toward the thoracic region, where it is lower, when the

pressures reverse during exhalation, the values prevent backflow of lymph. In

addition, when a lymphatic vessel distends, the smooth muscle, in its wall

contracts, which help move lymph from one segment of the vessel to the next.

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Role of Lymphatic System in Controlling Interstitial Fluid Protein Concentration,

Interstitial Fluid Volume, and Interstitial Fluid Pressure :

It is already clear that the lymphatic system functions as an “overflow

mechanism” to return to the circulation excess proteins and excess fluid volume from

the tissue spaces. Therefore, the lymphatic system also plays a central role in

controlling (1) the concentration of proteins in the interstitial fluids, (2) the volume of

interstitial fluid , and (3) the interstitial fluid pressure.

The small amounts of proteins leak continuously out of the blood capillaries

into the interstitium. Only minute amounts if any, of the leaked proteins return to the

circulation by way of the venous ends of the blood capillaries. Therefore, these

proteins tend to accumulate in the interstitial fluid, and this inturn increases the

colloid osmotic pressure of the interstitial fluids. The increasing colloid pressure in

the interstitial fluid shifts the balance of forces at the blood capillary membranes in

favor of fluid filtration into the interstitium. Therefore, fluid is pulled osmotically by

these proteins into the interstitium, thus increasing both the interstitial fluid volume

and the interstitial fluid pressure. The increasing interstitial fluid pressure greatly

increases the rate of lymph flow, as explained earlier. This inturn carries away the

excess volume and excess protein that has accumulated in the spaces.

Thus, once the interstitial fluid protein concentration reaches a certain level

and causes a comparable increase in interstitial fluid volume and interstitial fluid

pressure, the return of protein and fluid by way of the lymphatic system becomes

great enough the balance exactly the rate of leakage of these from the blood

capillaries. Therefore, the quantitative values of all these factors reach a steady state;

they will remain balanced at these levels until something changes the rate of leakage

of proteins and fluid from the blood capillaries.

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5. LOCAL CONROL OF BLOOD OF FLOW BY THE TISSUES AND HUMORAL REGULATION

Local Control of Blood Flow in Response to Tissue Need150 :

One of the most fundamental principles of circulatory function is the ability of

each tissue to control its own local blood flow in proportion to its metabolic needs.

Further more, as the need for blood flow changes, the flow follows the changes.

Some of the needs of the tissue for blood flow :

1. Delivery of oxygen to the tissues,

2. Delivery of other nutrients such as glucose, amino acids, fatty acids,

3. Removal of carbon dioxide from the tissues,

4. Removal of hydrogen ions from the tissues,

5. Maintenance of hydrogen ions from the tissues,

6. Maintenance of proper concentrations of other ions in the tissues,

7. Transport of various hormones and other specific substances to the different

tissues.

Variation in Blood Flow in Different Tissues and Oxygen :

In general, the greater the metabolism in an organ, the greater its blood flow.

Very large blood flows in the various glandular organs, for example, several hundred

ml/100 gm of thyroid or adrenal gland tissue and a blood flow of 95 ml/100 gm of

liver. The extremely large blood flow through the kidneys, 360 ml/min/100 gm. This

extreme amount of flow is required for the kidneys to perform their function of

cleansing the blood of the waste products.

On the other hand, most surprising is the low blood to the resting muscles of

the body, even though they constitute between 30-40 % of total body mass. In the

resting state, the metabolic activity of the muscles in very low, and so also is the

blood flow, only 4 ml/min/100 gm. Yet during heavy exercise, muscle metabolic

activity can increase more than 60-fold and the blood flow as much as 20-fold.

Mechanisms of Blood Flow Control :

Local blood flow can be divided into 2 phases :

(1) Acute Control

(2) Long-term Control.

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Acute control is achieved by rapid changes in local constriction of the

arterioles meta-arterioles, and precapillary sphincters, occurring within seconds to

minutes to provide a rapid means for maintaining appropriate local tissue blood flow.

Long-term control on the otherhand means slow changes in flow over a period of

days, weeks, or even months. In general, the long term changes provide for better

control of the flow in proportion to the needs of the tissues. These changes come

about as result of an increase or decrease in the physical sizes and numbers of actual

blood vessels supplying the tissues.

Acute Control of Local Blood Flow :

(I) Effect of tissue metabolism on Local Blood Flow :

An increase in metabolism upto 8 times normal increase the blood flow

acutely about fourfold. Once the metabolism rises high enough to remove

most of the nutrients form the blood, further increase in metabolism can occur

only with a concomitant increase in blood flow to supply the required

nutrients.

(II) Local Blood Flow Regulation when Oxygen Availability Changes :

One of the most necessary of the nutrients is oxygen. Whenever the

availability of oxygen to the tissues decreases, such as at high altitude, in

pneumonia, in carbon monoxide poisoning or in cyanide poisoning, the blood

flow through the tissues increases markedly.

There are two basic theories for the regulation of local blood flow when either

the rate of tissue metabolism changes or the availability of oxygen changes. They are

(1) The vasodilatory Theory

(2) The oxygen demand Theory

(1) The Vasodilatory Theory : Special role of adenosine :

According to this theory, the greater the rate of metabolism or the less the

availability of oxygen or some other nutrients to a tissue, the greater becomes

the rate of formation of a vasodilator substance. Most of the vasodilator

theories assume that the vasodilator substance is released from the tissue

mainly in response to oxygen deficiency. The decreased availability of oxygen

can cause both adenosine and lactic acid to be released from the tissues; these

substances can cause intense vasodilation. Some physiologists have suggested

that the substance adenosine is by far the most important of the local

vasodilators far controlling local blood flow. For instance, minute quantities of

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adenosine are released from heart muscle, whenever coronary heart flow

becomes too little.

(2) Oxygen Demand Theory for Local Blood Flow Control :

Although the vasodilator theory is accepted by most physiologists, several

critical facts have made a few physiologists favour still another theory, which

can be called either the oxygen demand theory. Oxygen is required to maintain

vascular muscle contraction. Therefore, in the absence of an adequate supply

of oxygen and other nutrients, it is reasonable to believe that the blood vessels

would naturally dilate. Smooth muscle requires oxygen to remain contracted,

one might assume that the strength of contraction of the sphincters would

increase with an increase in oxygen contraction. Consequently, when the

oxygen concentration in the tissue rises above a certain level, the precapillary

and meta-arteriole sphincters presumably would close and remain closed until

the tissue cells consume the excess oxygen. When oxygen concentration falls

low enough, the sphincters would open once more to begin the cycle again.

“Possible Role of Other Nutrients besides Oxygen in the Control of Local Blood

Flow” :

Under special conditions, it has been shown that lack of glucose in the

perfusing blood for longer than a few minutes can cause local tissue vasodilation.

Also it is possible that this same effect occurs when other nutrients, such as amino

acids or fatty acids, are deficient, although this has not been studied adequately. In

addition, vasodilation occurs in the vitamin deficiency disease, beriberi, in which the

patient usually has deficiencies of vitamin B substances thiamine, niacin and

riboflavin. In this disease, the peripheral vascular blood flow all over the body can

increase twofold, threefold. Because these vitamins are all concerned with the

oxidative phosphorylation mechanism for generating ATP in the local tissues. One

could suspect that deficiency of these vitamins leads to diminished smooth muscle

contractile ability and therefore to the local vasodilation.

Special Examples of “Metabolic” Control of Local Blood Flow :

(1) Reactive Hyperaemia

(2) Active Hyperaemia

(1) Reactive Hyperaemia :

When the blood supply to a tissue is blocked for a few seconds to several

hours and then is unblocked, the flow through the tissue usually increases to

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four to seven times normal; the increased flow will continue for a few seconds

if the block has lasted only a few seconds but sometimes for as long as many

hours if the blood flow has been stopped for an hour or more. This is called

“reactive hyperaemia”. After short periods of vascular occlusion, the extra

blood flow during the reactive hyperemia phase lasts long enough to repay

almost exactly the tissue oxygen deficit that has occurred during the period of

occlusion. This mechanism emphasizes the close connection between local

blood flow regulation and delivery of oxygen and other nutrients to the tissue.

(2) Active Hyperaemia :

When any tissue become highly active such as an exercising muscle,

gastrointestinal gland during a hyper-secretory period or even the brain during

rapid mental activity, the rate of blood flow through the tissue increases. The

increase in local metabolism causes the cells to devour the tissue fluid

nutrients extremely rapidly and also to release large quantities of vasodilator

substances, that results into dilate the local blood vessels and therefore, to

increase local blood flow.

Autoregulation of Blood Flow :

In any tissue of the body, an acute increase in arterial pressure will cause an

immediate rise in blood flow. Within less than a minute, the blood flow in most tissue

returns most of the way back toward the normal level. This return of flow back toward

normal is called “autoregulation of blood flow”. This is related to arterial pressure of

about 70 mm Hg and 175 mm Hg. The blood flow increases only to explain the acute

autoregulation mechanism - (1) Metabolic theory (2) Myogenic theory.

(1) Metabolic Theory : When the arterial pressure becomes too great, the excess

flow provides too much oxygen and too many other nutrients to tissues, and

these nutrients then cause the blood vessels to constrict and the flow to return

nearly to normal despite the increased pressure.

(2) Myogenic Theory : It is not related to tissue metabolism still it explains the

phenomenon of autoregulation. The sudden stretch of small blood vessels will

cause the smooth muscle of the vessel wall contract. When high arterial

pressure stretches the vessel, this inturn reduces the blood flow nearly back to

normal conversely, at low pressures, the degree of stretch of the vessel is less,

so that the smooth muscle releases and allows increased flow.

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It has been suggested especially that the myogenic mechanism protects the

capillaries form excessively high blood pressure. That is if the pressure in the small

arteriole rises too high, these vessels would simply constrict within seconds and

prevent this high pressure from been transmitted into the capillaries, which are so

weak that excessive pressure could rupture them.

Mechanism for Dilating the Large Vessels when Microvascular Blood Flow

increases the Endothelial Derived Relaxing Factor (Nitric Oxide):

The local mechanisms for controlling tissue blood flow can dilate only the

very small microvessels located in the immediate tissue itself because local feedback

caused by vasodilator substances or oxygen deficiency can reach only these vessels.

Yet, when blood flow through the microvascular portion of the circulation increases,

this entrains secondarily another mechanism that does dilate the larger arteries as

well.

The endothelial cells lining the arterioles and small arteries synthesize several

substances that, when released, can affect the degree of contraction of the arterial wll.

The most important of these is a vasodilator substance called “endothelial-derived

relaxing factor”, which is composed principally, if not entirely of nitric oxide, that has

a half life in blood only 6 seconds. Rapid flow of blood through the arteries causes

“shear-stress” on the endothelial cells because of viscous drag of the blood against the

vascular walls. This stress contorts the endothelial cells in the direction of flow and

causes greatly increased release of nitric oxide. The nitric oxide then releases the

arterial wall, causing it to dilate.

Multiple other stimuli also can cause nitric oxide to be released from the

endothelium. These stimuli include acetyl choline, bradykinin, ATP and others. The

nitric oxide inturn causes the local blood vessel to dilate.

Mechanism of Long Term Regulation change in Tissue Vascularity :

Over a period of hours, days and weeks, a long term type of local blood flow

regulation develops in addition to acute regulation. If a tissue becomes chronically

overactive and therefore, requires chronically increased quantities of nutrients the

blood supply usually increases within a few weeks almost to match the needs of the

tissue.

The mechanism of long term local blood flow regulation is a change in the

degree of vascularity of the tissues. That is if the arterial pressure falls to 60 mm Hg

and remains at this level for many weeks, the physical structural sizes of the vessels in

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the tissue increase and under some conditions, even the number of vessels increases.

On the other hand, if the pressure increases to a very high level, the number and sizes

of vessels decreases. If the metabolism in a given tissue is increased for a prolonged

period, vascularity increases, if the metabolism is decreased, vascularity decreases.

Thus there is reconstruction of the tissue vasculature to meet the need of the

tissues. This reconstruction occurs rapidly. It also occurs rapidly in new growth of

tissue, such as in scar tissue and in cancerous tissue. On the other hand, it occurs

slowly in old and well established tissue. Therefore, time required for long term

regulation to take place may be a only a few days in the neonate and years together in

elderly person. So response is greater in younger tissues than in older.

Role of Oxygen in Long Term Regulation :

Oxygen is important not only for acute control of local blood flow, but also

long term control. One of effect of this to increase the vascularity in the tissue of

many animals that live at high altitudes, where atmospheric oxygen is low. The excess

oxygen causes almost immediate cessation of new vascular growth in the retina, even

causes degeneration of capillaries that have already formed. There is explosive

overgrowth of new vessels to makeup for the sudden decrease in available oxygen.

Growth of New Vessels - Angiogenesis and Angiogenic Factors :

The term “angiogenesis” means growth of new blood vessels released from

the factors like

1. Ischaemic tissues

2. Tissue growing rapidly

3. Tissues having excessive high metabolic rate.

Multiple angiogenic factors have been found, where 3 of them have been best

characterized are (1) endothelial cells growth factor (2) fibroblast growth factor and

(3) angiogenin, which have been isolated from inadequate blood supply. So

deficiency of tissue oxygen and other nutrients lead to formation of angiogenic

factors.

They cause new vessels to sprout, either from small venules, occasionally

from capillaries. The first step is discontinuation of basement membrane of the

endothelial cells at point of sprouting, followed by rapid reproduction of new

endothelial cells, then streamout of vessel wall in extended cords directed towards

source of the angiogenic factors. The cells in each cord, continue to divide over into a

tube next. The tube connects with another tube, budding from another donor vessels

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and forms a capillary tubes through which blood begins to flow. If flow is more

smooth muscle cells eventually invade the wall. So that new vessels grow into small

arterioles are perhaps arteries. Thus angiogenesis explains the manner in which

metabolic factors in local tissue can cause growth of new vessels.

Development of collateral circulation :

When an artery, vein is blocked a new vascular channels develops around the

blockage and allows partial resupply of blood to the affect tissue. First stage in this

process is dilatation of vascular tubes around the point of blockage that already

connect the vessel above the blockage to the vessel below. This dilatation occurs

within the first minute or two initiating that it is simply a metabolic relaxation of

muscle fibres of the small vessels involved. After this initial opening of these

collateral vessels. The blood flow usually less than one quarter that needed to supply

tissue needs. The most important example of collateral vessel is thrombosis of one of

the coronary artery.

Humoral Regulation of the Circulation :

This means regulation of circulation by substances secreted or absorbed into

the body fluid such as hormones and ions. Some of these substances are formed by

special glands and transported into the blood throughout the entire body. There are

other substances formed in local tissue areas and cause only local circulatory effects.

Vasoconstrictor Agents –

Norepinephrine, Epinephrine :

Norepinephrine is powerful vasoconstrictor hormone. Epinephrine is some

what less even in some instances causes vasodilation. When the sympathetic nervous

system is stimulated in all parts of the body during stress or exercise. The sympathetic

nerve ending in individual tissue release norepinephrine that excites the heat, veins

and arterioles. The sympathetic nerves also cause adrenal medullae to cause secretion

both hormones into the blood. These hormones cause almost the same excitatory

effects on the circulation.

Angiotensin :

It is a powerful vasoconstrictor pressure. The effect of this is on small

arterioles real important of this is blood is that it normally act on all arterioles to

increase total peripheral resistance there by increasing the arterial pressure.

“Vasopressin” - it is also called as antidiuretic hormone, more powerful than

angiotensin released by posterior pituitary. It has important function in controlling the

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water reabsorption in renal tubules controlling body fluid volume so called anti-

diuretic hormone.

Endothelin :

it is a powerful vasoconstrictor in damaged blood vessels. This substance

present in endothelial cells of all blood vessels. This substance present in endothelial

cells of all blood vessels. The usual stimulus for release is damage to the endothelium

which prevents bleeding. A special function of endothelium might be constriction of

umbilical artery of a neonate immediately after birth.

Vasodilator Agents :

Bradykinin :

Several substances called kinins cause vasodilatation formed in the blood and

tissue fluid. Bradykinin causes powerful arteriolar dilatation and increased capillary

permeability. It is believed that bradykinin play a role in regulating blood flow of

skin. Salivary gland, gastrointestinal glands.

Serotonin :

In can have either vasodilator or vasoconstrictor effect. Depending upon the

condition of are of circulation. Its function is still clear.

Histamine :

It is released by every tissue of body, when it becomes damaged or inflamed.

It is derived from mast cells or basophils. It has got powerful vasodilator effect

allowing leakage of fluid and plasma protein into the tissue.

Prostaglandins :

Almost every tissue of the body contain prostaglandins. These are important

intracellular effects.

Effects of Ions on Vascular Control :

Many different ions have little function in regulation of circulation. An

increase in calcium ion concentration causes smooth muscle contraction. So acts as

vasoconstrictor. An increase in potassium ion contraction inhibits smooth muscle

contraction. Magnesium ions have also get same effect. An increase in sodium ion

concentration causes arteriole dilatation.

Nervous Regulation of Circulation: 53

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Nervous control normally adjusts blood flow tissue by. Nervous control

mainly affects more global function such as redistributing the blood flow to different

areas of the body, increasing pumping action of heart and providing rapid control of

arterial pressure. Sympathetic and parasympathetic nervous system are important in

contributing to regulation of heart function.

Sympathetic Nervous System :

Sympathetic vasomotor nerve fibres leave the spinal cord through all thoracic

and first two lumbar spinal nerves. They pass into the sympathetic chain and to the

circulation. Through specific sympathetic nerves innervating vasculature of internal

viscera and heart. And through the spinal nerves which innervates vasculature of

peripheral areas. Sympathetic fibres innervating meta-arterioles. The innervation of

veins makes possible for the sympathetic stimulation to decrease the volume of these

vessels. So it is playing major role in regulation of cardio-vascular function

stimulation markedly increases the heart rate.

Parasympathetic Nervous System :

They play minor role regulation of circulation. Parasympathetic stimulation

causes marked decrease in heart rate and slight decrease in heart muscle contractility.

Role of Nervous System for Rapid Control of Arterial Pressure :

Sympathetic nerve are stimulated to cause entire vasoconstrictor and

cardioaccelator function at the same time. There is inhibition of parasympathetic

nerves. This can occur in these ways :

1. Almost all arterioles of the body are constricted increasing peripheral

resistance concretely arterial pressure to provide run-off of blood

2. The veins are also strongly constricted displacing towards heart, thus

increasing the volume of blood in heart chambers.

3. Sympathetic nerves have direct effect to increase the contractile force of the

heart muscle increasing the capable of heart pump.

Reflex Mechanism for Maintaining Normal Arterial Pressure :

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Barareceptor Mechanism :

Baroreceptors are spray type nerve endings lying in the walls of arteries

(Large arteries) stimulated when they are stretched. The baroreceptors respond

extremely, to changes in arterial pressure. Excitation of baroreceptors by pressure in

arteries reflexly causes the arterial pressure to decrease providing decreased

peripheral resistance in cardiac output (Fig 18.5)

Chemoreceptors :

Chemoreceptors are sensitive to oxygen lack, carbon dioxide excess and

hydrogen ion excess. They are located in several organs. The signals transmitted from

chemoreceptors into vasomotor centres elevate arterial pressure. Special Features of Nervous Control of Arterial Pressure :

Skeletal muscles and nerve play important role in controlling circulation.

Abdominal Compression Reflex :

Any factors stimulate sympathetic vasoconstrictor system, nerve signals are

transmitted simultaneously through skeletal nerves through skeletal muscles of the

body. This increases basal tone of the muscle which compresses all venous reservoirs

to translocate blood towards the heart.

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6. REGIONAL VENOUS SYSTEM

VEINS OF HEAD AND NECK :

Most blood draining from the head passes into three pairs of veins. The

internal jugular, external jugular, and vertebral veins. With in the brain, all the veins

drain into dural venous sinuses and then into the internal jugular veins. Dural venous

sinuses are endothelial lined venous channels between layers of the cranial dura

mater.

Internal Jugular Veins : [Fig. 6 (a)]

The flow of blood from the dural venous sinuses into the internal jugular veins

is as follows –

The superior sagittal sinus begins at the frontal bone, where it receives a vein

from the nasal cavity, and passes posteriorly to the occipital bone. Along its course, it

receives blood from the superior, medial and lateral aspects of the cerebral

hemispheres, meninges, and cranial bones. The superior sagittal sinus usually turns to

the right and drains into the right transverse sinus. The inferior sagittal sinus is much

smaller that the superior sagittal sinus; it begins posterior to the attachment of the falx

cerebri and receives the great cerebral vein to become the straight sinsus. The great

cerebral vein drains to deeper parts of the brain. Along its course the inferior sagittal

sinus also receives tributaries from the aspects of the cerebral hemisphere.

The “Straight Sinus” runs in the tentorium cerebelli and is formed by the

union of the inferior sagittal sinus and the great cerebral vein. The straight sinus also

receives blood from the cerebellum and usually drains into the left transverse sinus.

The “Transverse Sinuses” begin near the occipital bone, pass laterally and

anteriorly, and become the sigmoid sinuses near the temporal bone. The transverse

sinuses receive blood from the cerebrum, cerebellum and cranial bones.

The “Sigmoid Sinuses”(S shaped) are located along the temporal bone. They

pass through the jugular foramina, where they terminate in the internal jugular veins.

The sigmoid sinuses drain the transverse sinuses.

The “Cavernosus Sinuses” (cave like) are located on either side of the

sphenoid bone. They receive blood from the ophthalmic veins from the orbits, and

from the cerebral hemispheres. They ultimately empty into the transverse sinuses and

internal jugular veins. The cavernous sinuses are unique because they have nerves and

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a major blood vessel passing through them on their way to the orbit and face. The

occulomotor nerve, trochlear nerve, and ophthalmic and maxillary braches of the

trigeminal nerve as well as internal carotid arteries pass through the cavernosus

sinuses. The right and left internal jugular veins pass inferiorly on either side of the

neck lateral to the internal carotid and common carotid arteries. They then unite with

the subclavian veins posterior to the clavicle at the sternoclavicular joints to form the

right and left brachio-cephalic veins. From here blood flows into the superior vena

cava. The general structures drained by the internal jugular veins are the brain, face

and neck.152

External Jugular Veins: 153

The external jugular vein mainly drains the scalp and face, although it also

drains some deeper parts. The vein is formed by the union of the posterior division of

the retromandibular vein with the posterior auricular vein and begins near the

mandibular angle just below or in the parotid gland. It descends from the angle to the

middle clavicle, running obliquely, superficial to the sternocleidomastoid, to the root

of the neck. Here it crosses deeper fascia and ends in the subclavian vein, lateral or

anterior to scalneus anterior. There are valves at its entrance into the subclavian, but

they do not prevent regurgitation. Its wall is adherent to the aim of the fascial

opening. It is covered by platysma, superficial fascia and skin and is separated from

sternocleidomastoid by deep cervical fascia. The vein crosses transverse cutaneous

nerve and lies parallel with great auricular nerve, posterior to its upper half. In size the

external jugular vein is inversely proportional to the other veins in the neck, and may

be double. Between the entrance into the subclavian vein and a point 4 cm above the

clavicle, the vein is often dilated, producing a so called sinus.

Posterior-external Jugular Vein :

The posterior external jugular vein begins in the occipital scalp, and drains the

skin and the superficial muscles which lie posterior superior in the neck. It usually

joins the middle part of the external jugular vein.

Anterior Jugular Vein :

The anterior jugular vein arises near the hyoid bone from the confluence of the

superficial submandibular veins. It descends between the midline and the anterior

border of sterno-cleido mastoid.

Turning laterally, low in the neck, deep to the sternocleidomastoid but

superficial to the infrahyoidstrap muscle, it joins either the end of the external jugular

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vein or may enter the subclavian vein directly. In size it is usually inverse to the

external jugular vein. It communicates with the internal jugular vein. There are

usually two anterior jugular veins, united just above the manubrium by a large

transverse jugular arch, receiving the inferior thyroid tributaries. They have no valves

and may be replaced by a middle trunk.

Venous Drainage of the Brain: 154

The venous drainage of the brain occurs through a complex system of deep

and superficial veins. Theses veins possess no valves and have thin wall devoid of

muscular tissue. They pierce the arachnoid matter and the thinner layer of the dura

mater to open into the dural venous sinuses.

Veins of the Brainstem :

The veins of brainstem form a superficial venous plexus deep to the arteries.

Veins of medulla oblongata drain into the veins of spinal cord or the adjacent dural

venous sinuses or into the variable radicular veins which accompany the last four

cranial nerves to either the inferior petrosal or occipital sinuses, or to the superior bulb

of the jugular vein.

Veins of Cerebellum :

The veins of the cerebellum drain mainly into sinuses adjacent to them or from

the superior surface, into the great cerebral vein. The cerebellar veins course on the

cerebellar surface, and comprise superior and inferior groups.

Veins of the Cerebral Hemisphere :

External and internal cerebral veins drain the surfaces and the interior of the

cerebral hemisphere. External cerebral veins may be divided into three groups,

namely, superior, middle and inferior.

Eight – twelve superior cerebral veins drain the supero-lateral and medial

surfaces of each hemisphere. They mainly follow the sulci, although some do pass

across gyri. They ascend to the super-medial border of the hemisphere, where they

receive small veins from the medial surface, and then open into the superior sagittal

sinus. The larger posterior veins are directed obliquely forwards, against the direction

of flow in the sinus, an arrangement which may resist their collapse when intracranial

pressure is raised.

The internal cerebral vein drains the deep parts of the hemisphere and the

choroids plexuses of third and lateral ventricles. It is formed near the interventricular

foramen, behind the column of the fornix.

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Veins of Vertebrae: 155

Veins of the vertebral column form intricate plexuses along the entire column,

external and internal to the vertebral canal. Both groups are devoid of valves,

anastomose freely with each other, and join the intervertebral veins. Inter-connections

are widely established between these plexuses and longitudinal veins early in fetal

life.

The veins also communicate with cranial dural venous sinuses and with the

deep veins of the neck and pelvis. The venous complexes associated with the vertebral

column can dilate considerably and can form alternate routes of venous return in

patients of with major venous obstruction in the neck, chest or abdomen. The absence

of valves allows pathways for the wide and sometimes para-abdominal spread of

malignant diseases and sepsis. Pressure changes in the body cavities are transmitted

into these venous plexuses and thus to the CSF, though the cord itself may be

protected from such congestion by valves in the small veins which drain from the cord

into the internal vertebral plexus. External vertebral venous plexuses, basi-vertebral

veins and inter-vertebral are the veins found in vertebrae.

Veins of the Face: 156

The veins of the face are subject to considerable variations, and therefore, the

following description concerns those which are relatively constant.

Supratrochlear Vein :

The supratrochlear vein starts on the forehead from a venous network

connected to the frontal tributaries of the superficial temporal vein. Veins from the

network form a single trunk, descending near the midline parallel with its fellow or

single trunk, descending near the midline parallel with its fellow the bridge of the

nose. Each vein is joined by a nasal arch across the nose. The veins then diverge, each

joining a supra-orbital vein to form the facial vein near the medial canthus of the eye.

Supra-orbital Vein :

The supra-orbital vein begins near the zygomatic process of the frontal bone,

connecting with the branches of the superficial and middle temporal veins. It passes

medially above the orbital opening pierces the orbicularis oculi and unites with the

supra-trochlear vein near the medial canthus of the eye to form the facial vein. A

branch passes through the supra-orbital notch to connect with superior ophthalmic

vein. In the notch it receives veins from the frontal sinus and frontal diploe.

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Facial Vein :

The facial vein is the main vein of the face. After receiving the supratrochlear

and supra-orbital veins, it travels obliquely downwards by the side of the nose passes

under zygomaticus major, resorius and platysma, descends to the anterior border and

then passes over the surface of masseter. It crosses the body of the mandible, and runs

in the neck to drain into the internal jugular vein. The uppermost segment of the facial

vein – above its junction with the superior labial vein is also termed the angular vein.

The facial vein initially lies behind the more tortuous facial artery, but crosses it at the

lower border of the mandible. The fact that the vein lacks, and that it is connected

with cavernous sinus of the considerable clinical significance in terms of the spread of

infection.

Tributaries of Facial Vein :

Near its origin, the facial vein connects with superior ophthalmic vein, both

directly and via the supraorbital vein, and so is linked to the cavernous sinus. The

facial vein receives tributaries from the pterygoid venous plexuses. It also receives the

inferior palpebral, superior and inferior labial, buccinator, parotid and masseteric

veins, and other tributaries which join it below the mandible.

Superficial Temporal Vein :

The superficial temporal vein begins in a wide spread network joined across

the scalp to the contra-lateral vein and to the ipsi-lateral supra-trochlear, supra-orbial,

posterior auricular and occipital veins that ll drain the some network. Anterior and

posterior tributaries unite above the zygomatic arch to form the superficial temporal

vein. Accompanying its artery, the vein crosses the posterior root of the zygoma and

enters the parotid gland. Here, the superficial temporal vein joins the maxillar vein, to

form the retro-mandibular vein.

Tributaries :

The tributaries are the parotid veins, rami draining the tempero-mandibular

joint, anterior auricular veins and the transverse facial vein. The middle temporal

veins receives the orbital vein and passes back between layers of temporal fascia,

which it pierces to join the superficial temporal vein just above the level of the

zygomatic arch.

Buccal, Mental and Infra-orbital Veins :

The buccal, menal and infra-orbital veins drain the cheek and chin regions and

pass into the pterygoid venous plexus.

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Posterior Auricular and Occipital Veins :

The posterior auricular vein arises in parieto-occipital network that also drains

into tributaries of the occipital and superficial temporal veins. It descends behind the

auricle to join the posterior division of the retro-mandibular vein in or just below the

parotid gland to form the external jugular vein. It receives a stylomastoid vein and

tributaries from the cranial surface of the auricle, drains the region of the scalp behind

the ear and drains into the eternal jugular vein. The occipital vein begins in a posterior

network in the scalp, pierces the cranial attachment of the trapezius turns into the

suboccipital triangle and joins the deep cervical and vertebral veins.

Lingual Vein: 157

The lingual veins follow two routes. The dorsal lingual vein drain the dorsum

and sides of the tongue, join the lingual vein accompanying the lingual artery between

hypoglossus and genioglossus, and enter the internal jugular near the tip of the tongue

and runs back, lying near the mucous membrane. On the inferior surface of the

tongue, near the anterior border of hypoglossus it joins a sublingual vein, from the

sublingual salivary gland, to form the venae comitans nervi hypoglossi which runs

back between mylohyoid and hypoglossus with the hypoglossal nerve to join the

facial, internal jugular or lingual vein.

Pharyngeal Veins :

The pharyngeal veins begin in a pharyngeal plexus external to the pharynx.

They receive meningeal veins and a vein from the pterygoid canal, and usually end in

the internal jugular vein, but may sometimes end in the facial, lingual or superior

thyroid vein.

Superior Thyroid Vein :

The superior thyroid vein is formed by deep and superficial tributaries

corresponding to the arterial branches in the upper part of the thyroid gland. It

accompanies the superior thyroid artery receives the superior laryngeal and crico-

thyroid veins, and ends in the internal jugular or facial vein.

Middle Thyroid Vein :

The middle thyroid vein drains the lower part of the gland and also receives

veins from the larynx and trachea. It crosses anterior to the common carotid artery to

join the internal jugular vein behind the superior belly of omohyoid.

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Vertebral Vein :

Numerous small tributaries from internal vertebral plexuses leave the vertebral

canal above the posterior arch of the atlas and join small veins from local deep

muscles in the sub-occipital triangle. Their union produces a vessel which enters the

foramen in the transverse process of the atlas and forms a plexus around the vertebral

artery. It descends through successive transverse foramina and ends as the vertebral

vein. The vein emerges from the sixth cervical transverse foramen, where it descends,

at first anterior, then antero-lateral, to the vertebral artery, to open supero-posteriorly

into the brachio-cephalic vein.

As it descends it passes behind the internal jugular vein and in front of the first

part of the subclavian artery. A small accessory vertebral vein usually descends from

the vertebral plexus, traverses the seventh cervical transverse foramen and turns

forwards between the subclavian artery and the cervical pleura to join the brachio-

cephalic vein.

Superficial Veins of Upper Limb: 158

Superficial veins of the upper limb assume importance in medical practice

because these are most commonly used for intravenous injections and for

withdrawing blood for transfusion or for testing. [Fig. 7 (d)]

1. Host of the superficial veins of the limb join together to form the two large

veins, cephalic and basilic. An accessory cephalic vein is often present.

2. The superficial veins run away from pressure points. Therefore, they are

absent in the palm in the ulnar border of the forearm and in the back of the

arm and trapezius region. This makes the course of the veins spiral, from the

dorsal to the ventral surface of the limb.

3. The pre-axial vein is longer than the post axial. In other words, the pre-axial

vein drain into the deep vein more proximally that the post-axial vein which

becomes deep in the middle of the arm.

4. The earlier a vein becomes deep the better the because the venous return is

then assisted by muscular compression. The load of the pre-axial vein is

greatly relieved by the more efficient post-axial (basilica) through a short

circulating channel [median cubital vein] and partly also by the deep veins

through a performator vein connecting the median cubital with deep vein.

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5. The superficial veins are accompanied by cutaneous nerves and superficial

lymphatics, and not by arteries. The superficial lymph nodes lie along the

veins, and the deep lymph nodes along the arteries.

6. The superficial veins are best utilized for intravenous infections.

Cephalic Vein :

The cephalic vein forms over the anatomical snuff-box from the radial

extremity of the dorsal venous plexus. It runs proximally over the distal lateral aspect

of the radius where it is easily visible.

Cephalic vein is the pre-axial vein of the upper limb. It runs upwards through

the roof of the anatomical suff-box winds round the lateral border of the distal part of

the forearm. It continues upwards in front of the elbow and along the lateral border of

the biceps brachis. Then it pierces the deep fascia at the lower border of the pectoralis

major. It pierces the clavipectoral fascia and joins the axiallary vein.

At the elbow, the greater part of its blood is drained into the basilic vein

through the median cubital vein, and partly also into the deeps veins through the

perforator vein.

It is accompanied by the lateral cutaneous nerve of the forearm, and the

terminal part of the radial nerve.

Basilic Vein :

The basilic vein of each upper limb originates in the medial part of the dorsal

venous arch. It is the post-axial vein of the upper limb. It extends along the posterior

surface of the ulna to the point near the elbow where it receives the median cubital

vein.

It runs upwards :

1. Along the back of the medial border of the forearm.

2. Winds around the border near the elbow.

3. Continuous upwards in front of the elbow and along the media margin of the

biceps brachi upto the middle of the arm where it pierces the deep fascia.

4. And runs along the medial side of the brachial artery upto the lower border of

the major where it becomes the axillary vein.

It is accompanied by the posterior brach of the medial cutaneous nerve of the

forearm and the terminal part of the dorsal branch of the ulnar nerve.

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Deep Veins: 159

The venae comitantes running with the radial and ulnar arteries drain the deep

and superficial palmar venous arches respectively. They unite near the elbow as

paired brachial veins. The radial veins are smaller, and receive the deep dorsal veins

of the hand. The ulnar veins drain the deep palmar venous arch, and connect with

superficial veins near the wrist. Near the elbow they receive the venae comitantes and

a large branch connects them to the median cubital vein. [Fig. 7 (e)]

1. Radials : Radial veins receive the dorsal metacarpal veins

2. Ulnars : Ulnar veins receive tributaries from the palmar venous arch. Radial

and ulnar veins unite in the bend of the elbow to form the brachial veins.

3. Brachials : Located on either side of the brachial arteries, the brachial veins

join into the axiallary veins. 4. Axiallary veins : The axiallary vein is the continuation of the basilic vein. The

axillary vein is joined by the venae comitantes of the brachial artery a little

above the lower border of the teres major. It lies on the medial side of the

axillary artery. The outer border of the first rib it becomes the subclavian vein.

In addition, to the tributaries corresponding to the branches of the axillary

artery, it receives the cephalic vein in its upper part.

There is no axiallary sheath around the vein, which is free to expand during

times of increased blood flow. Occasionally a muscular band called the axilary arch

overlies the vein. It may compress the vein and cause spontaneous thrombosis.

Subclavian Vein: 160

Right and left subclavian vein unite with the internal jugular to form the

brachio-cephalic veins. The thoracic duct of the lymphatic system delivers lymph into

the left subclavian vein at the junction with the internal jugular. The right lymphatic

duct delivers lymph into the right subclavian vein at the corresponding.

The subclavian vein is a continuation of the axillary vein. It extends from the

outer border of the first rib to the medial border of scalenus anterior, where it joins the

internal jugular to form brachio-cephalic vein. The clavicle and subclavius are

anterior, and the subclavian artery is postero-superior, separated by scalenus anterior

and the phrenic nerve. The first rib and pleura are inferior. The vein usually has a pair

of valves 0.2 cm from its end. Its tributaries are the external jugular, dorsal scapular

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and anterior jugular veins, and occasionally a small brach from the cephalic vein,

which ascends anterior to the clavicle. At its junction with the internal jugular vein,

the left subclavian receives the thoracic duct; the right subclavian vein receives the

right lymphatic duct.

Medial Cubital Vein: 161

Medial cubital vein is a large communicating vein which shunts blood from

cephalic to the basilic vein. If vein must be punctured for an injection, transfusion, or

removal of a blood sample, the median cubital veins are preferred.

It begins from the cephalic vein 2.5 cm below the bend of the elbow, runs

obliquely upward and medially, and ends in the basilic vein 2.5 cm above the medial

epicondyle. It is separated from the brachial artery by the biciptal aponeurosis.

It may receive tributaries from the front of the forearm and is connected to the

deep veins through a perforator vein which pierces the bicipital aponeurosis. The

perforator vein fixes the median cubital vein and thus makes it ideal for intravenous

injections.

Median Vein of the Forearm :

Median vein of the forearm begins from the palmar venous network, and ends

in any one of the veins in front of the elbow. Sometimes it divides into median

cephalic and median basilic veins which join the cephalic and basilic veins

respectively.

Dorsal Venous Arch :

Dorsal venous arch lies on the dorsum of the hand. Its afferents include :

1. three dorsal metacarpal veins,

2. a dorsal digital vein from the medial side of the little finger.

3. a dorsal digital vein from the radial side of the index finger

4. two dorsal digital veins from the thumb,

5. most of the blood from the palm through veins passing around the margins of

the hand and also by perforating veins passing through the interosseuss spaces.

Superficial Veins of The Hand: 162

Dorsal and Palms Digital Veins : [Fig. 7 (c)]

Dorsal digital veins pass along the sides of the fingers, joined by oblique

braches. They unite from the adjacent sides of the digits into three dorsal metacarpal

veins, which form a dorsal venous network over the metacarpus. This is joined

laterally by a dorsal digital vein from the radial digital veins of the thumb, and is

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prolonged proximally as the cephalic vein. Medially and dorsal digital vein from the

ulnar side of minimus joins the network, which ultimately drains proximally into the

basilic vein. A vein often connects the central parts of the network to the cephalic

vein near midforearm.

Palmar digital veins connect to their dorsal counterparts by oblique

intercapitullar veins which pass between metacarpal heads. They also drain to a

plexus superficial to the palmar aponeurosis, extending over both thenar and

hypothenar regions.

Deep Veins of the Hand :

Superficial and deep palmar venous arches accompany their arterial

counterparts and receive the corresponding braches. Thus common palmar digital

veins join the superficial arch, and palmar metacarpal veins join the deep arch.

Palmar and Dorsal Metacarpal Veins :

Deep veins accompanying the dorsal metacarpal arteries receive perforating

branches from the palmar metacarpal veins. They end in the radial veins and the

dorsal venous network over the metacarpus. This network is joined laterally by a

dorsal digital vein from the radial side of the index finger and by both digital veins of

the thumb. It is prolonged proximally as the cephalic vein.

Veins of the Thorax 163

Superior Vena Cava : [Fig. 6 (b)]

The superior vena cava is 7 cm in length, formed by the junction of the

brachio-cephalic veins. It returns blood to the heart from the superior half of the body.

It begins behind the lower border of the first eight costal cartilage near the sternum,

descends vertically behind the first and second intercostals spaces, and ends in the

upper right atrium behind the third right costal cartilage. Its inferior half is within the

fibrous pericardium, which it pierces level with the second costal cartilage. Covered

antero-laterally by serous pericardium, it is slightly covex to the right. It has no

valves.

Tributaries :

The azygos vein and small veins from the pericardium and other mediastinal

structures.

Inferior Vena Cava :

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The inferior vena cava conveys the blood to the right atrium from all structure

below the diaphragm. The majority of its course is within the abdomen, but a small

section lies within the fibrous pericardium in the thorax. It is formed by the junction

of the common ilial veins anterior to the fifth lumbar vertebral body, a little to its

right.

It ascends anterior to the vertebral column, to the right of the aorta. It is

contained is a deep groove on the posterior surface of the liver or sometimes is a

tunnel completed by a band of liver tissue. It crosses the tendinous part of the

diaphragm between its median and right ‘leaves’ and inclines slightly anteromedially.

Passing through the fibrous pericardium and through a posterior inflexion of the

serious pericardium, it opens into the infero-posterior part of the right atrium. The

abdominal portion of the inferior vena cava is devoid of valves.

The abdominal inferior vena cava usually receives the common iliac veins at

its origin and the lumbar, right gonadal, renal, right supra-renal, inferior phrenic and

hepatic veins during its course.

The thoracic part is very short, partly inside and partly outside the pericardinal

sac. The extrapericardial part is separated from the right pleura and lung by the right

phrenic nerve. The intrapericardinal part is covered, except posteriorly, by inflected

serous pericardium. The venous drainage from the tissues below the diaphragm finally

ends in the inferior vena cava. The inferior vena cava of traverses the diaphragm at

the level of the eight and ninth thoracic vertebra between the right and central tendon

of the diaphragm. It then passes through the pericardium and drains into the right

atrium.

Brachiocephalic Veins: 164

Right Brachio-cephalic veins :

About 2.5 cm long the right brachio-cephalic vein begins posterior to the

sternal ends of the right clavicle, and descends almost vertically to join the left

brachio-cephalic vein, forming the superior vena cava posterior to the lower border of

the first right costal cartilage, near the right sternal border. Its tributaries are the right

vertebral, internal, thoracic, inferior thyroid and sometimes the first right posterior

intercostal veins.

Left Brachio-cephalic vein :

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Some 6 cm long, the left brachio-cephalic vein begins posterior to the sternal

end of the left clavicle, anterior to the cervical pleura. It descends obliquely to the

right, posterior to the upper half of the manubrium sterni, to the sternal end of the first

right costal cartilage, uniting here with the right brachio-cephalic vein to form the

superior vena cava. Its tributaries are the right vertebral, internal thoracic, inferior

thyroid, superior intercostal, sometimes the first left posterior intercostal, thymic and

pericardial veins.

Azygos System :

The azygos system, besides collecting blood from the thorax and abdominal

wall, may serve as bypass for all the inferior vena cava that drains blood from the

lower body. Several small veins directly like the azygos system of the inferior vena

cava or hepatic portal vein becomes obstructed, the azygos system can return blood

from the lower body to the superior vena cava.

Azygos Vein :

The azygos vein is anterior to the vertebral column, slightly to the right of the

midline. It usually begins at the junction begins at the junction of the right ascending

lumbar and right subcostal veins near the diaphragm. At the level of the 4th thoracic

vertebra, it arches over the root of the right lung to end in the superior vena cava.

Generally, the azygos vein drains the right side of the thoracic wall, thoracic viscera

and abdominal wall. Specifically the azygos vein receives blood from most of the

right posterior intercostals, hemiazygos, accessory hemiazygos, oesophageal,

mediastinal, pericardial and bronchial veins.

Hemiazygos vein :

The hemiazygos vein is anterior to the vertebral column and slightly to the left

of the midline. It usually begins at the junction of the left ascending lumbar and left

subcostal veins. It terminates by joining the azygos vein at about the the level of the

ninth thoracic vertebra. Generally the hemiazygos vein drains the left side of the

thoracic wall, thoracic wall, thoracic viscera and abdominal wall. Specifically, the

hemiazygos vein receives blood from the ninth through the eleventh left posterior

intercostals, esophageal, mediastinal and sometimes the accessory hemiazygos vein.

Accessory Hemiazygos Vein :

The accessory hemiazygos vein is also anterior to the vertebral column and to

the left of the midline. It begins at four intercostal space and descends from the fifth

to the eighth thoracic vertebra or ends in the hemiazygos vein. It terminates by joining

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the azygos vein at about the level of the eighth thoracic vertebra. The accessory

hemiazygos vein drains the left side of the thoracic wall. It receives blood from the 4th

through eighth left posterior intercostal veins, left bronchial, and mediastinal veins.

Veins of Abdomen And Pelvis: 165

Blood from the abdominal and pelvic viscera and abdominal wall returns

to the heart via the “inferior vena cava”. Many small veins enter the inferior vena

cava. Most carry return flow from the parietal braches of the abdominal aorta, and

this names correspond to the names of the arteries. [Fig. 7 (b)]

The inferior vena cava doesn’t receive veins directly from the gastro-intestinal

tract, spleen, pancreas, and gall bladder. These organs pass their blood into a common

vein, the hepatic portal vein, which delivers blood to the liver. The superior

mesenteric and splenic veins until to form the hepatic portal vein. This special flow of

venous blood is called hepatic portal circulation.

Inferior Vena Cava :

The two common iliac veins that drain to lower limbs, pelvis and abdomen

unite to form the inferior vena cava. The inferior vena cava extends superiorly

through the abdomen and thorax to the right atrium.

Common Iliac Veins :

The common iliac veins are formed by the union of the internal and external

iliac veins anterior to the sacroiliac joint and represent the distal continuation of the

inferior vena cava at their bifurcation. The right common iliac vein is much shorter

than the left and is also more vertical. Generally, the common iliac veins drain the

pelvis, external genitals, and lower limbs.

Internal Iliac Veins :

The internal iliac veins begins near the superior portion of the greater sciatic

notch and run medial to their corresponding arteries. Generally the veins drain the

thigh, buttocks, external genitals and pelvis.

External Iliac Veins :

The external iliac veins are companions of the internal iliac arteries and begin

at the inguinal ligaments as continuations of the femoral veins. They end anterior to

the sacroiliac joint where they join with the internal iliac veins to form the common

iliac veins. The external iliac veins drain the lower limbs, cremaster muscle in males

and the abdominal wall.

Lumbar Veins :

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A series of parallel lumbar veins, usually four on each side, drain blood from

the both sides of the posterior abdominal wall, vertebral canal, spinal cord and

meninges. Lumbar veins run horizontally with the lumber arteries. The lumbar veins

connect at right angles with the right and left ascending lumbar veins, which form the

origin of the corresponding azygos or hemiazygos vein. The lumbar vein drain blood

into the ascending lumbars and then run to the inferior vena cava, where they release

the remainder of the flow.

Gonadal Veins :

The gonadal veins ascend with gonadal arteries along the posterior abdominal

wall. In the male the gonadal veins are called the testicular veins. The testicular veins

drain the testes. In the female, the gonadal veins are called ovarian veins. The ovarian

veins drain the ovaries. The left ovarian vein empties into the left renal vein, and the

right ovarian vein drains into the inferior vena cava.

Renal Veins :

The renal veins are large and pass anterior to the renal arteries. The left renal

vein is longer than the right renal vein and passes anterior to the abdominal aorta. It

receives the left testicular, left inferior phrenic, and usually left supra-renal veins. The

right renal empties into the inferior vena cava posterior to duodenum. The renal veins

drain kidneys.

Supra-renal veins :

These vein drain the adrenal glands.

Veins of the Lower Limb: 166

The veins of the lower limb can subdivided, like those of the upper limb, into

superficial and deep groups. The superficial veins are subcutaneous and lie in the

superficial fascia; the deep veins accompany the major arteries. Both groups have

valves, which are more numerous in the deep veins and also more numerous than in

the veins of the upper limb. Venous plexuses occur within and between some of the

lower limb muscles. [Fig. 7 (a)]

The principal named superficial veins are the long and short saphenous veins.

Their numerous tributaries are mainly unnamed.

Deep veins of the lower limbs accompany the arteries and their branches.

Plantar digital veins arise from plexuses in the plantar regions of the toes, connect

with dorsal digital veins and unite four plantar meta-tarsal veins. These run in the

intermetatarsal spaces and connect by perforating veins with dorsal veins then

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continue to form a day plantar arterial arch. From this arch, medial and lateral plantar

veins run near the corresponding arteries. They communicate with the long and short

saphenous veins before forming the posterior tibial veins behind medial malleolus.

The posterior tibial veins accompany the posterior tibial artery. They receive

veins from the calf muscles, especially the venous plexus in soleus, and connect the

with superficial veins and with the peroneal veins. The latter, running with their

artery, receive branches from soleus and superficial veins.

The anterior tibial veins are continuations of venae comintantes of the dorsalis

pedis artery. They leave the extensor region between the tibia and fibula, pass through

the proximal end of the interossoeus membrane, and unite with the posterior tibial

veins to form the popliteal vein at the distal border of popliteus.

Considerable of the venous drainage is of great importance because in the

lower limb venous blood has to ascend against gravity. This is aided by a number of

local factors, the failure of which gives rise to varicose veins. The veins of lower limb

may be classified into three groups. 167

I. Superficial Veins

II. Deep Veins

III. Perforating Veins

(I) Superficial Veins :

They include the great and small saphenous veins and their tributaries. They

lie in the superficial fascia, on the surface of the deep surface. They are thick walled

because of the presence of smooth muscle and some fibrous and elastic tissues in their

walls.

(II) Deep Veins :

These are the anterior and posterior tibial, peroneal, popliteal, & femoral veins

and their tributaries. They accompany the arteries, and are supported by powerful

surrounding muscles. The valves are more numerous in deep veins than in superficial

veins. They are more efficient channels than the superficial veins because of the

driving force of muscular contraction.

(III) Perforating Veins :

They connect the superficial with the deep veins. Their valves permit only one

way flow of blood, from the superficial to the deep veins. There are about five

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perforators along the great saphenous vein, and one perforator along the small

saphenous vein.

Superficial Veins of Lower limb :

(1) The dorsal venous arch lies on the dorsum of the foot over the proximal part

of the meta-tarsal bones. It receives four dorsal meta-tarsal veins each of

which is formed by the union of two dorsal digital veins

(2) The great or long saphenous vein is formed by the union of the medial end of

the dorsal venous arch with the medial marginal vein which drains the medial

side of the medial surface of tibia obliquely, and runs along its medial border

to reach the back of the knee. The saphenous nerve runs in front of the great

saphenous vein.

(3) The small or short saphenous vein is formed by the union of the lateral end of

the dorsal venous arch with lateral marginal vein, draining the lateral side of

the little toe. It passes upwards behind the lateral malleolus to reach the back

of the leg. The sural nerve accompanies the small saphenous vein.

Both saphenous veins are connected to the deep veins through the perforating

veins.

Great or Long Saphenous Vein: 168

Saphes Easily seen.

The saphenous vein can be easily seen in the leg. Venous drainage acquires

importance as blood has to flow up against the gravity. [Fig. 7 (b)]

The long saphenous vain, is the largest and longest superficial vein of the

lower limb. It starts on the dorsum of the foot from the medial of the dorsal venous

arch, and runs upwards in front of the medial malleolus along the medial side of the

leg, and behind the knee. In the thigh, it inclines forwards to reach the saphenous

opening where it pierces the cribriform fascia and opens into the femoral vein.

In its course through the thigh the long saphenous vein is accompanied by the

branches of the medial femoral cutaneous nerve. Before piercing the cribriform fascia,

it receives three named tributaries corresponding to the 3 cutaneous arteries and also

many unnamed tributaries.

It contains about 10-15 valves which prevent back flow of the venous blood,

which tends to occur because of gravity. One valve is always present at the saphenous

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femoral junction. Incompetence of these valves makes the vein dilated and tortuous

leading to varicose vein.

In almost its entire extent the vein lies in superficial veins, but it has many

connections with the deep veins, especially in the leg. The veins is also connected to

the deeps veins of the limb by perforating veins. There are three medial perforators

just above the ankle, one perforator just below the knee and another one in the region

of the adductor canal. The perforating veins are also provided with valves which

permit flow of blood only from the superficial to deep vein.

Tributaries :

At the ankle the long saphenous vein drains the sole by medial marginal veins.

In the leg it often connects with the short saphenous vein and with deep veins via

perforating veins. Just distal to the knee it usually receives three large tributaries from

the front of the leg, from the tibial malleolar region and from the calf. The tributary

draining the tibial malleolar region is formed delicate veins overt the medial malleolus

and then ascends the medial aspect of the calf as the posterior arch vein.

It connects with posterior tibial venae comintantes by a series of perforating

veins. These are usually three equally spaced between the medial malleolus and the

mid calf. More than three such perforators are uncommon and an arch vein perforators

above mid calf is only very rarely found.

Above the posterior crural arch vein, perforating veins join the long saphenous

vein, or one of its main tributaries at the two main sites. The first is at a level in the

upper calf indicated by its name, the tibial tubercle. Perforator; the second is in the

lower / intermediate third of the thigh where it perforates the deep fascial roof of the

subsartorial canal to join the femoral vein.

In the thigh the long saphenous vein receives many tributaries. Some open

independently, whilst others converge to form large named channels that frequently

pas forwards the basal half of the femoral triangle before joining the long saphenous

near its termination. These may be grouped as follows : one or mor large postero-

medial tributaries, one or more large antero-medial tributaries, four or more peri-

inguinal veins. The postero-medial vein of the thigh, large and sometimes double,

drains a large superficial region indicated by its name. It has radiological and surgical

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significance. One of its lower radicles is often continuous with short saphenous vein.

The postero-medial vein is sometimes named the accessory saphenous vein, through

some restrict the term accessory to a lower, postero-medial tributary when tow are

present. Another large vessel, the antero-lateral vein of the thigh usually commences

from an anterior network of veins in the distal thigh and crosses the apex and distal

half of the femoral triangle to reach the long saphenous vein. As the latter traverses

the saphenous opening, it is joined by the superficial epigastric, superficial circumflex

iliac and superficial external pudendal veins. Their mode of union varies. Superficial

epiagastric and circumflex iliac veins drain the inferior abdominal wall, the latter also

receiving tributaries from the proximo-lateral region of thigh. The long saphenous

vein is often harvested for grafts used both in peripheral and coronary arterial surgery.

Surface Marking of Saphenous Vein: 169

It can be marked by joining the following points, although it is easily visible in

living subjects :

(a) First point on the dorsum of foot at the medial end of the dorsal venous arch

(b) Second point on the anterior surface of the medial malleolus

(c) Third point on the medial border of the tibia at the junction of the upper two

thirds and lower one third of the leg

(d) Fourth point at the adductor tubercle

(e) 5th point just below the centre of the saphenous opening.

Its formation on the dorsum of the foot, its course along the entire length of

the lower limb, and its termination into femoral vein. It contains about 10-20 valves.

There is one valve that lies just before the vein pierces the cribriform fascia and

another at its termination into the femoral vein.

Short Saphenous Vein:170

The short saphenous vein starts on the lateral side of the foot and ascends up

on the back of the leg to end in the popliteal vein. The vein is formed on the dorsum

of the foot by the union of the lateral end of the dorsal venous arch with the lateral

marginal vein. In lower third of the calf it ascends lateral to the calcaneal tendon,

lying on the deep fascia and covered only by superficial fascia and skin. In the leg it

ascends lateral to the tendocalcaneus, and then along the middle line of the calf, to the

lower part of the popliteal fossa. Here it pierces the deep fascia and opens into the

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popliteal vein. It drains the lateral border of the foot, the heel and the back of the leg.

It is connected with the great saphenous and with deep veins.

Tributaries :

The short saphenous vein connects with deep veins on the dorsum of the foot,

receives many cutaneous tributaries in the leg, and sends several communicating

branches proximally and medially to join the long saphenous vein. Sometimes a

communicating branch ascends medially to the accessory saphenous vein. This may

be main the continuation of the short saphenous vein. In the leg, the short saphenous

vein lies near the sural nerve, it has 7-13 valves one near its termination. Its mode of

ending is variable, it may join the long saphenous vein in the proximal thigh or it may

bifurcate, one branch joining the long saphenous, the other the popliteal or deep

posterior femoral veins. Sometimes, it ends distal to the knee in the long saphenous or

sural muscular vein.

Surface Marking :

It can be marked by joining the following points, although this vein is also

easily visible in its lower part :

(a) A point on the dorsum of the foot at the lateral end of the dorsal venous arch

(b) Second point behind the lateral malleolus.

(c) Third point just lateral to the tendocalcaneous above the lateral malleolus.

(d) Fourth point at the centre of the popliteal fossa.

Its formation on the dorsum of the foot, course along the back of the leg, and

termination into the popliteal vein.

Just before piercing the popliteal fascia, it may give a communicating branch

to the accessory saphenous vein. Sometimes, the whole of the small saphenous vein

opens into the great saphenous vein through the accessory saphenous vein.

Occasionally, the small saphenous vein ends below the knee either in the great

saphenous vein, or in the deep muscular veins of the leg.

Perforating Veins: 171

As already mentioned, they connect the superficial with the deep veins. There

are classified as follows :

(I) Indirectly Perforating Veins :

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Indirect perforating veins connect the superficial veins with the deep veins

through the muscular veins.

(II) Direct Perforating Veins :

Direct perforating veins connect the superficial veins directly with deep veins.

The great and small saphenous veins are the large direct perforators.

(a) In the thigh : the adductor canal perforator connects the great saphenous vein

with the femoral vein in the lower part of the adductor canal.

(b) Below the knee : one perforator connects the great saphenous vein or the

posterior arch vein with the posterior tibial vein.

(c) In the leg : (i) a lateral perforator is present at the junction of the middle and

lower third of the leg. It connects the small saphenous vein or one of its

tributaries with peroneal vein. Medially, there are three perforators which

connect the posterior arch vein with the posterior tibial vein.

(d) The upper medial perforator lies at the junction of the middle and lower thirds

of the leg.

(e) The middle medial perforator lies above the medial malleolus.

(f) The lower medial perforator lies posteroinferior to the medial malleolus.

Deep Veins of Lower Limb: 172

(I) Posterior Tibial Veins :

The posterior tibial veins accompany the posterior tibial artery. They receive

tributaries from the calf muscle and connections from the superficial veins and

the peroneal veins. Posterior tibial vein is formed by the union of the medial

and lateral plantar veins posterior to the medial malleolus.

(II) Anterior Tibial Veins :

The anterior tibial vein is the superior continuation of the dorsalis pedis vein

in the foot. It extends between the tibia and fibula and unites with the posterior

tibial to form the popliteal vein at the distal border of the popliteus.

Popliteal Vein: 173

It begins at the lower border of the popliteus by the union of veins

accompanying the anterior and posterior tibial arteries, and posterior tibial arteries. It

is medial to the popliteal artery in the lower part of the fossa; posterior to the artery in

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the middle and postero-lateral to it in the upper part of the fossa. The vein continues

as the femoral vein at the opening in the adductors magnus.

The popliteal vein receives -

(1) the small saphenous vein and

(2) the vein corresponding to the branches of the popliteal artery.

Profunda Femoris Vein :

The profunda femoris vein lies anterior to its artery, and has tributaries

corresponding to the branches of the artery. Through these tributaries it connects

distally with the popliteal and proximally with the inferior gluteal veins. It sometimes

drains medial and lateral circumflex femoral veins. It has a valve just before it

terminates.

Femoral Vein: 174

The femoral vein accompanies its artery beginning at the adductor opening, as

the continuation of the popliteal vein, and ending posterior to the inguinal ligament as

the external iliac vein. In the distal adductor canal, it is postero-lateral to the femoral

artery, more proximally in the canal, and in the distal femoral triangle, it is posterior

to it, proximally, at the base of the triangle, it is medial. The vein occupies the middle

compartment of the femoral sheath, between the femoral artery and canal, fat in the

latter allowing expansion of the vein. It has many muscular tributaries; 4-12 cm distal

the inguinal ligament the profunda femoris vein joins it posteriorly and then the long

saphenous vein, which enters anteriorly. Veins accompanying the superficial

epigastric, superficial circumflex iliac and external pudendal arteries join the long

saphenous vein before it enters the saphenous opening. Lateral and medial circumflex

femoris veins are usually tributaries of the femoral. There are usually four or five

valves in the femoral vein. The two most constant are just the distal to the entry of the

profounda femoris and near the inguinal ligament.

Deep and Superficial Venous Systems of the Foot: 175

Plantar digital veins arise from the plexuses in the plantar regions of the toes,

connecting with dorsal digital veins and uniting into four plantar metatarsal veins. The

latter run in the intermetatarsal spaces and connect by perforating veins with dorsal

veins, then continue to form the deep plantar venous arch that accompanies the plantar

arterial arch. From this venous arch, medial and lateral plantar veins run near the

corresponding arteries and after communicating with the great and small saphenous

veins, from the posterior tibial veins behind the medial malleolus.

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The principal named superficial veins are the great and small saphenous. Their

numerous tributaries are mostly unnamed.

Dorsal digital veins receive rami from the plantar digital veins in the clefts

between the toes and then join to form dorsal metacarpal veins, which are united

across the proximal parts of the metatarsal bones in a dorsal venous arch. Proximal to

this arch, an irregular dorsal venous network receives tributaries from deep veins and

is continuous, proximally with a venous network in the leg. At each side of the foot,

this network connects with medial and lateral marginal veins, which are both formed

mainly by veins from more superficial parts of the sole. In the sole, superficial veins

form a plantar cutaneous arch across the roots of the toes and also drain into the

medial and lateral marginal veins. Proximal to the plantar arch there is a plantar

cutaneous venous plexus, especially dense in the fat of the heel. It connects with the

plantar cutaneous venous arch and other deep veins, but drains mainly into the

marginal veins. The veins of the sole are an important part of the lower limb ‘venous

pump’ system aiding return of the blood up the limb. Intermittent to enhance this flow

and so reduce the risk of deep vein thrombosis during periods of increased risk, e.g.

after surgery.

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7. BLOOD LETTING

The importance of blood letting as medicinal agent, in comparison with other

means of cure in various respects, it is the equivocal of remedies when properly

administered. In short, “blood letting is a remedy which when judiciously employed it

is hardly possible to estimate to highly”. Different methods are in use for taking away

the blood for therapeutic purposes first by (1) phlebotomy – where blood is drawn

from available veins. (2) Arteriotomy – where artery is punctured (3) Scarification –

Scraping of superficial cells with syringe. Venesection or phlebotomy is much more

effective than any other modes of treatment for an instance the object may be to take

away the blood so rapidly to make a great impression on the system. 176

Likewise in modern era also Phlebotomy (Venesection) is part of treatment.

Performed in different conditions like – polycythemia vera, hemochromotosis,

hepatitis B, hepatitis C and C C F. 177

Phlebotomy :

Phlebo vein, tome to cut.

Venesection :

Opening of a vein for withdrawal of blood. Although phlebotomy is a

synonym for venesection in clinical practice, phlebotomy refers to therapeutic blood

letting, such as removing some blood to lower the viscosity of blood of a patient with

polycythemia. 178

Webster’s defines phlebotomy as phle bot omy / Fli-bat-eh-mee\n: The letting

of blood in the treatment of diseases. i.e. VENESECTION.111

Historical Background of Blood Letting Therapy :

The practice of blood letting seemed logical when the foundation of all

medical treatment was based on four body humours blood,, phlegm, yellow bile and

black bile. Health was thought to be restored by purging, vomiting, blood letting etc.

The art of blood letting was familiar before Hippocrates in fifth century B.C. Both

surgeons and barbers were practicing this blood letting. Blood letting came to the U.S.

in 18th and early 19th century. The first U. S. president George Washington died from

throat infection in 1799 where he had been drained of nine pints of blood in 24 hours,

where one pint =16-30 ounces, when patient becomes faint bleeding was often

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encouraged in large areas of the body by multiple incisions. But by the end of 19

century this phlebotomy was declared. 180

The practice of blood letting or phlebotomy dates back to antiquity. The

followers of Hippocrates in blood letting in th 5th century B.C. strongly believed in

blood letting. Early Egyptian have been inspired by seeing bats and remove blood

from animals. Hyppos scratches on tree until the bleed , and other animals scratching

at diseased part for relief. Additionally many human examples of bleeding such as

nasal bleeding, haemetemesis , rectal bleeding, menstruation – these science in nature

led early civilians to think that bleeding must have some beneficial value.

From these simple observation came increasingly the complex theories as to

why blood letting is necessary and how it worked? In early theory of four bodily

humours, an imbalance in these humours was postulated as need for a blood letting

was used to treat everything from fever, madness, upto anemia as one can imagine

treating an anemic patient by removing more blood was the best of ideas. Through the

middle ages to 18th century. There were many strides in medieval field regarding

diseased state, anatomy and therapeutic majors.

Blood letting in modern medicine referred to as phlebotomy was a popular

medical practice upto the late 19th century. It was one of oldest medical practices in

Greeks, Egyptians, and Mesopotamia. It was theorized by many disease caused by

plethoras (over abundance in the blood), so advised that these plethoras be treated

initially by excessive, sweating, reduced food intake, meeting and blood letting,

Greek physicians practiced phlebotomy extensively and gained reputation. Greek

physician Gallen believed that blood was the dominant humor in the order to balance

the other humors. So he also preferred blood letting, he created a complex system that

how much blood should be removed based on patient age, constitution, season,

symptoms etc. The blood to be let was of a specific nature determined by the disease,

either capillaries or venous, and close area of body was affected the linked different

blood vessels with different organs according to their supposed drainage. Ex: right

medial cubital vein in the right hand would be let for liver problems. 181

Blood Letting in the Last Millennium :

Even after the humoral system fell into disuse, but the practice of blood letting

was often recommended by physican and carried out by surgeons and barbers. Blood

letting was used to treat a wide range of diseases becoming a standard treatment for

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every element. The practice continued throughout the middle ages. In Northern

Europe, Netherlands, France, physicians advocated frequent phlebotomy throughout

18th century the efficiency of phlebotomy was hotly debated, but in 19th century it has

been restricted to few diseases. 182

Phlebotomy is longest running tradition in medical field, originated in

civilization of Egypt, Greek period flourished in Arabic and Indian medicine practice

continued for 2500 years until it was replaced by modern medicine. There are

references of phlebotomy for pneumonia, fevers, back pain, fractures, wounds. This is

based on ancient Indian medicine in which blood considered as one of the humour

maintaining health. It was not until well into the 19th century that people began to

question a value of blood letting. So later phlebotomy is almost never used any more

except for certain rare conditions; one is hemochromatosis. 183

For many centuries blood letting was considered a tried and true remedy for

certain conditions. It was recommended for fevers, inflammations, a rarity of disease

conditions and ironically for hemorrhage. Although it fell in and out of favour, it

persisted in to the 20th century and was even recommended by Sir William Osler in

1923 edition in his principles and practice of medicines. 184

Preparation :

Patients having their blood drawn for analysis may be asked to continue

medications are avoid food. Patients donating blood will be asked for brief medical

history with hematocrit value Hb%, ESR, etc.

Blood letting was popular practice from antiquity to the late 19th century. This

phlebotomy is act of drawing or removing blood from the circulating system through

a cut or puncture.

Description: 185

Phlebotomy is performed by a technician or phlebotomist, blood is usually

taken from a vein on the back the hand or inside of the elbow. The skin over the area

is wiped with an antiseptic, an elastic band, is tied over the hand. The bands acts like

tourniquet, slowing the blood flow in the arm and making the veins more visible. The

patient is asked to make a first and technician feels. The veins in order to select an

appropriate one. When vein is selected the technician inserts a needle into the vein

and releases the elastic band. The required amount of blood drawn and needle is

withdrawn from the vein. The patients pulse and blood pressure should be monitored.

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The amount of blood depends upon the purpose of phlebotomy. Blood donors usually

contribute around 350 ml in a session. But in therapeutic phlebotomy larger amount of

blood is drawn than the blood donation.

General Considerations :

1. Open needle package but don’t remove needle shield thread needle on to

holder.

2. Select needle, tubes appropriate for sample desired and a sterile container.

3. Tubes that contain additives should be gently tapped to dislodge any additive

which may be trapped around the stopper.

4. Inster tube into holder push tube stopper onto needle until leading edge of

stopper meets guidelines of holder. Tubes were retract slightly. Leave in the

position. When using 13 mm diameter tubes, it is important to enter the tubes

in the holder when penetrating the stopper to preclude sidewall penetration

and resultant loss of volume.

5. Select site for venipuncture.

6. Apply tourniquet. Prepare venipuncture site with an appropriate antiseptic.

Don’t palpate venipuncture site after cleansing.

7. Place patients arm in a downward position.

8. Remove needle shield. Perform venipuncture with arm in a downward position

and tube stopper uppermost.

9. Push tube onto holder, puncturing diaphragm of stopper.

10. Remove tourniquet as soon as blood appear in tube. Donot allow content of

tube to contact. The stopper or the end of the needle during procedure. If no

blood flows into tube or ceases to flow before an adequate sample is collected,

the following steps are suggested to complete satisfactorily.

Collection : Confirm correct position of needle cannula in vein.

If a multiple sample needle is being used, remove, the tube and place a new

tube into the holder, if the second tube does not draw, remove the needle and

discard an appropriate disposal device. Repeat procedure from Step-I.

11. When first tube in full and blood flow ceases, remove it from holder.

12. Place succeeding tubes in holer, puncturing diaphragm to initiate flow. Tube

without additives are drawn before tubes with additives.

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13. While each successive tube is fillup, invert the previous tube containing

additives 8-10 times don’t flow. Vigorous mixing can cause hemolysis.

14. As soon as blood stops flowing in the last tube, remove needle from vein,

apply pressure to puncture site with dry, sterile swab, until bleeding stops.

15. Applying bandage is desired.

16. After the venipuncture, the top of the stopper may contain residual blood at the

puncture site. Proper precautions should be taken when handling tubes to

avoid contact with blood droplets. Dispose of any holder that becomes

contaminated with blood.

17. Needle disposal.

After Care :

When blood is drawn and needle is removed pressure is placed on punctured

site with a cotton wool, to stop bleeding bandage is applied. It is not uncommon for a

patient to feel dizzy or noisiated during after phlebotomy. The patient may be

encouraged to rest for a short period after completion of procedure. Patients are also

instructed to drink plenty of fluids and to eat regularly to replace lost blood volume.

Patients who experience swelling of the puncture site are continued bleeding after

phlebotomy should get medical help.

Most patients will have a small bruise or mild soreness at the puncture site for

several days. Therapeutic phlebotomy may cause thrombocytosis (a vascular

condition characterized by high platelet count) and chronic iron deficiency, some

patients. The risks can be minimized by use of sterilized equipments, careful

attention, and proper techniques.

Significance of Phlebotomy :

1. Recently, in modern medical science blood letting by venesection

(phlebotomy) advised in the conditions like acute pulmonary oedema,

thrombosis of the cerebral arteries, right heart failure indicated by orthopnoea

with distended jugular veins, cyanosis, venous congestion, in acute

pericarditis, in lobar pneumonia where the patients is cyanosed, uraemia

etc.The venesection is done 5-20 ounces of blood is letted out provided there

should not be severe anaemia. 188

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2. In iron over load states blood letting is the choice of treatment such as in

hemochromoatosis, tranferrin, deficiency, porphyria, erythropoeitc siderosis,

after portacaval shunting a large quantities of blood is removed about 500 ml

weekly for one – two years, upto the fall of hemoglobin and serum ferritin

level. 189

3. In an alcoholic iron absorption is increased in small intestine. Multiple factors

contribute to hepatic iron deposition, which is a contributing factor for

development of cirrhosis and hepatitis C is always co-factor for the

development of cirrhosis in an alcoholic.190

4. Blood letting is effective in elimination of amino transferase levels of patients

with chronic hepatitis C and iron overload.191

5. When the circulation of blood was first discovered at the same time effects of

blood letting would be clearly understood. The effects of blood letting were

judged upon certain pimple, as if the blood were removing from the veins. The

contractibility of vessels, vital property is improved. 192

6. Hakim Mohammad Ghyas is one of the practioners of India who is practicing

and appreciated effect of blood letting to cure variety of ailments. He claims

blood letting can cure arthritis, lumbago and cancer. The basic tenet of therapy

is the belief that impure blood is the cause of all ailments, get rid of the bad

blood and get well. Even if several session may be needed to achieve the goal. 193

7. In certain conditions management is replaced by venesection such as CCF,

where there is increased strain on right ventricle. So by phlebotomy total

volume of blood is lessened. The work of heat is lightened for a time. The

some result also we can get in pneumonia, pleurisy and bronchitis. It also

helps to lower blood arterial tension in early stages of cerebral hemorrhage

when heart is working vigorously venesection may lead to lowering the blood

pressure and so giving a blood in ruptured vessels an opportunity to coagulate.

In various convulsive attacks, acute uraemia, blood letting in beneficial.

8. Blood letting, by phlebotomy lead to improvement in peripheral insulin

sensitivity in inviduals with high infertility type-2 diabetes.

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9. Formation of blood cells appear in yolk sac of the two week embryo. By 8

weeks in established by liver of embryo, by 16 weeks liver has become major

sight of blood cells formation. Spleen also active during this period. Lymphoid

cells and foetal thymus is the temporary sight of lymphocytes. Highly cellular

bone marrow becomes an active blood making system about 20 weeks. At

birth active blood making red marrow occupies upto 22 years. Adult blood

marrow has a large reserve capacity for cell production, whenever there is

excessive demand liver, spleen make the blood.

10. In old age red marrow is replaced by inactive yellow marrow. So red marrow

forms all types of blood cells and also active in destruction of R.B.C.

Therefore, red marrow is the most active organs of the body. It is generally

accepted that all blood cells made from a relatively few cells capable of

mitosis. The production of R.B.C’s referred as erythropoesis.

In health, erythropoesis is regulated from bone marrow and is

stimulated by hypoxia (lack of oxygen). However, oxygen lack does not act

directly on haemopoetic tissues, where it stimulated production of

erythropoetic hormone. Erythropoetin is fromed in kidney also by the action of

erythropoetic factor “erythrogenin”. It is present in kidneys released into the

blood in response to hypoxia. Thyroid hormones T.S.H, adrenocorticoids,

andreno-corticotrophic hormones, human growth hormone – all promote

erythropoietic formation and enhance R.B.C. formation. So in

hypothyroidism, there is reduced erythropoesis. Polycythemia (excess R.B.C.

production) is feature of Cushing syndrome. However high dose of steroids

inhibit erythropoesis. Male hormones stimulate, female hormone depressed by

erythropoietic response.

11. A physiological secondary polycythemia is as a result of tissue hypoxia. In

diseases like chronic bronchitis, emphysema, C.C.F. and Fallot’s tetrology.

Oxygen carrying capacity of blood is increased by polycythemia, where there

is increased viscosity of blood. Increased viscosity produces raised blood

pressure. Venesection is sometimes employed to reduce the red cell volume. 194

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12. Haemochromatosis is an autosomal recessive disease characterized by an

increase in iron absorption relative to body iron stores. It has a prevalence of

one in 300 in the Australian Caucasian community. Symptoms and signs are

related to the amount of body iron stores. Early symptoms include lethargy

and fatigue, whilst late symptoms are related to the organs affected such as

liver, heart, pancreas and pituitary gland. Cirrhosis of liver is a particularly

important complication because it is associated with a 200-fold higher risk of

heptocellular carcinoma. On the other hand, the extra risk is entirely removed

if the patient is diagnosed and treated before cirrhosis develops. 195

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DISCUSSION

Discussion is one of prime importance to constitute, the proper conclusions in

any type of research. Science is always subjected for change. It is always relative

truth, not absolute truth. On the other hand, Ayurved is greatly emphasized on its

classical texts, Aptha Vachanas by ancient Acharyas. These are always truths, as they

have done observations and documented, their experiences for the welfare of

mankind. The concepts are evolved many years ago, because of generation gap and

lack of interpretation, concepts are not passed onto future generation properly. So now

we are lacking the opportunity to understand and to clarify the doubts. So the present

study was carried out to ‘anatomically locate Shakhagata Vedhya Sira Sthanas in

particular diseases (literary research). So that the concepts of Sira Shareera and Sira

Vyadha Vidhi Shareera can be better understood and to pass on knowledge to the

future generation for its practical utility.

Discussion on Sira Shareera :

The term ‘Sira, Dhamani’ are as old as Vedas. They have been generally used

with common meaning. But these are not synonymous. Of course, in general Siras

means blood vessels. But on the basis of interpretation of commentators ‘Dhamanis’

is a channel connected to the heart which is thick and ‘Sira’ is thin blood vessels.

Rather than Sushruta, Charaka in clear about this text with quoting dictum “Dhmanat

Dhamanyaha, Sravanath Srotansi, Saranat Sira”. ‘Dhma’ means pumping of Rasa by

heart into Dhamanis, ‘Sru’ means channels where there is slow discharge of fluid.

‘Sra’ means root of word ‘Sira’ means to move slowly. So with these points view,

Dhamanis are arteries, Siras are veins and Srotas are lymphatics. As per Gangadhar

Shastri, the classification of Sira can be understood like this.

Veins are playing very important role in both pulmonary and systemic

circulation. These are characterized by large capacitance compared to arteries.

Initially they were considered as simply reservoirs of blood. But now it has been

identified as veins are very essential to maintain proper circulation, cardiac output

drainage and venous return in the mechanism of homeostasis. The blood vessels like

arteries, veins and capillaries have got similar structural component with little

difference. Compared to arteries veins are thin walled, elastic tissue is less, but in

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artery walls are thick with excess elastic muscle fibers. Microscopically it has got

three layers – 1. tunica intima; it is made up of endothelium performing diffusion,

fibrinolysis, growth of new cells and circulation of lymphocytes, 2. – tunica media ;

this is a thin layer of smooth muscle in veins with properties like distensibility,

elasticity, rigidity, 3. – tunica adventitia; it is formed by general connective tissue

with varying thickness.

TABLE NO. 14 SHOWING CLASSFICATION OF SIRAS ACCORDING TO VARNA

Siraprakara Sirakarya Tridosha Drushtya

Vargikaraa 1 Rohinyaha Nourishing body by Upasnehana &

Anugrahana

Artery –

Pittavahi

2 Neela Nourishing body by Upasnehana &

Anugrahana

Veins –

Pittavahinya

3 Gourya Nourishing body by Upasnehana &

Anugrahana

Lymphatics –

Kaphavahinya

4 Aruna Akunchana Prasaranadi Karmas Autonomic Nerves –

Vatavahinya

The vein are capable of constricting and dilating, thereby storing small or

large quantity of blood and making this blood available for circulation. Venous return

will regulate cardiac output. The pressure of the veins is very important in circulatory

functions. Usually four to seven mm of Hg. The valves of the veins are arranged in

the direction of blood flow, i.e. towards the heart. As it act as a blood reservoir, when

there is a blood loss, arterial pressure begins to fall, inturn, send sympathetic nerves

signals to the veins causing them to constrict, so that the reserved blood in the vein

comes into the circulation.

Discussion on Siravyadha Vidhi Shareera :

Siravyadha is significant therapeutic tool, when judiciously administered. To

denote its importance, Sushruta has himself explained that ‘Siravyadham

Chikitsardham Shalya Tantra Prakirtitaha Yada Pranitaha Samyak Basti

Kayachikitsite’. Half of the health hazards can be managed by Siravyadha as Rakta is

being chief causative factor in the manifestation of diseases. So Raktamokshana by

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different modalities is much more effective in resolving pathogenesis. There are many

historical evidences where it was extensively practiced. During the procedure

preoperatively, indication and contraindication are analyzed. Instruments are collected

depending on the wisdom of the surgeon, site, disease and available instruments.

Sushruta has encouraged modification of instruments as per necessity. Operatively,

patient is taken in particular position, vein of the site should become prominent.

According to the diseases and their Adhisthana different Siras are selected for

Vyadhana. As per Sushruta’s explanation, as he is expert of Rachana Shareera. In

classics, it has been advocated that the blood letting should be done when

environment should not be too cold or too hot; because environmental stimuli can

cause Heena-Mithya-Ati Srava of Rakta. During the procedure it is necessary to

decide the quantity of blood to be letted out. As per classics, one Prastha (768 ml) has

been advocated which is Uttama Shodhana. But in general condition of the patients,

Hb% of the blood, severity of the diseased condition, quantity may be altered to half

Prastha (384 ml) or quarter Prastha (192 ml). Automatic stoppage of blood after

certain time is an indication of Samyak Siravyadha, associatedly the patient feels light

and severity of illness is decreased.

Siravyadha will be beneficial to maintain good health by causing Varna,

Prasannata, Agnideepti, Vegapravrutti, Tushti, Pushti. All Rakta Pradoshaja Vikaras

are successfully treated. According to present day researches it has been identified

that blood letting by phlebotomy is useful in many diseased conditions like acute

pulmonary oedema, thrombosis of cerebral arteries, orthopnoea, venous congestion,

percarditis, pneumonia, iron overload, hemochromatosis, alcoholic liver diseases,

hepatitis C, lumbago, cancer, arthritis, neuritis, type-II diabetes, CCF etc.

In general, the various probable mechanisms are going to change in body by

blood letting, such as local blood supply is improved, local metabolism is improved,

local drainage system is improved, fresh RBCs are produced which are active.

Hepato-cellular activity is improved by enzymatic activity by release of hormones,

sympathetic nerve function improved, as it directly stimulates bone marrow, immune

related T-lymphocytes are produced. Because of these, Siravyadha Vidhi Shareera has

got its own importance on the basis of scientific background.

Discussion on Correlative Study :

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Raktamokshana is one of the important para-surgical procedure denoting

letting of impure blood outside the body. Different modalities of Raktamokshana can

be adopted, but Siravyadha is one of the Shastravacharana. Of course, it appears to be

surprising that different sites have been advocated in different diseases. Why can’t

common site is selected in all diseases?, is the point interpreted here to analyze this

context, different hypothesis and patho-physiological mechanisms are applicable as

the basic unit of the body is cell. Each cell is especially adopting different mechanism

to perform functions. So the term ‘homeostasis’ is used to denoted maintenance of

constant conditions in internal environment. The function of circulation is to serve the

needs of the tissues such as nutrients, oxygen, hormones and also transport waste

products away. When tissues are active they need more blood flow. Heart normally

cannot increase its cardiac out more than four to seven times. Therefore, it is not

possible to increase the blood flow everywhere in the body. When a particular

demands increased flow, instead micro-vessel of each tissue are monitoring the tissue

needs, such as availability of oxygen and nutrients and the accumulation of waste

products, these inturn control local blood flow to the level of tissue need. The

microcirculation of each type tissue of body is specially organized to serve special

needs. Every cell have got their own microcirculation to maintain its constant internal

environment.

On the basis of this general information, the dictum of Sushruta is found to be

suitable. So that according to Roga Adhisthana, different sites of Siravyadha is

selected in different diseases, such as in Padadaha, Visarpa, Chippa, Vatarakta,

Vatakantaka, Vicharchika, Padadari – ‘Two Angula above from Kshipra Marma’-

medial metatarsal vein (a branch of dorsal venous arch).

In Vataja Shleepada – ‘four Angula above the Gupha Sandhi’- short saphenous vein.

In Pittaja Shleepada – ‘four Angula the Gulpha Sandhi’ – branch of dorsal venous

arch. In Kaphaja Shleepada – ‘four Angula above the ‘Kshipra Marma’ – branch of

dorsal venous arch. In Kroshtuka Shirsha, Khanja and Pangu – ‘four Angula above

from Gulpha Sanhi’- short saphenous vein. In Apachi – ‘two Angula below from

Indrabasti Marma’ – tributaries of short saphenous vein. In Grudhrasi – ‘four Angula

above or below from Janu Sandhi’ – great saphenous vein. In Galaganda – ‘Urumula

Sthita Sira’ – femoral vein.

In Pleehodara – ‘Vama-Kurpara Sandhi Sthita Sira’ or ‘Sira present in Vama

Kanistika and Anamika Angulis’ – left median cubital vein or branch of metacarpal

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vein. In Yakruddalyudara – ‘Dakshina Kurpara Sandhisthita Sira’ – right median

cubital vein. In Vishwachi – ‘four Angula above the Kurpara Sandhi’ – cephalic vein.

In Apachi – ‘two Angula below from Indrabasti Marma’ – basilic vein.

Interpretation on Clinical Applicability of Siravyadha

Sthanas in Lower and Upper limbs :

As per the literary review, the concept of Shodhana therapy in Ayurveda in

concerned, always Doshas should be removed from nearest routes. Example, in

Vatadusti – Basti, in Pittadusti – Virechana, in Kaphadusti - Vamana, which is

depending upon their Mulasthanas. Likewise, as Raktamokshana is also one of the

Shodhana therapy, so it is recommended to remove the vitiated blood from nearest

route of Roga Adhisthana. It has been considered that Rakta is Mula of Shareera,

responsible for health, where its Dusti causes various illness. So Sthanika

Raktamokshana has been advised in different diseases. So different modalities of

Raktamokshana is indicated in many diseases, where Siravyadha is significant of

them.

So the sites of Siravyadha dealt by Sushruta is only with the aim of that

Dushita Rakta should be expelled out from Sameepastha Marga. With this motive he

might have been told particular sites for Siravyadha in particular diseased conditions.

He has recommended only Siras which are superficially situated on the contrary,

contraindicated the Vyadhana of Siras deeply situated Srias as Avedhya Siras. On the

basis of said principles, Sushruta might have been told particular Vyadhana Sthana in

different disease conditions. The truths documented by the practically ancients scholar

Sushruta on the basis of his experiences and superimposed power, can never be

rejected, unless the concepts thought in their point of views, so that, that can be better

understood and analyzed on basis of present existing modern science also.

When we have reviewed anatomy, physiology, circulation, venous systems,

homeostasis on the grounds of literary principles, the sites of Siravyadha dealt by

Sushruta are found to be correct, as blood letting from particular site is effective in

resolving the pathology of diseased conditions and beneficial in neutralizing

physiological mechanisms by various changes in the body. As the body has got its

own capacity to compensate during blood loss, performing many defense actions to

resolve pathology and to maintain homeostasis. Cellular level changes have been

brought by various metabolic changes, neurological changes, hormonal changes. As

the blood is circulating in the closed circuit, providing oxygen, nutrients, hormones

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and carry out metabolic waste products. Every cell has got its own control to fulfill

the needs itself.

Concerned to diseases conditions in ‘Padadaha’ – which is nothing but

burning sensation of feet that is due to decreased utilization of pyruvic acid by tissues

due to any cause. So accumulation of pyruvic acid in tissue spaces leads to Padadaha.

Here, blood letting is done in Padadaha i.e. two Angula above from Kshipra Marma,

which is noting but metatarsal vein of dorsal venous arch. One of the most

fundamental principles of circulatory function is the ability of each tissue to control

its own blood flow in proportion to its metabolic needs. In general, the greater the

metabolism, greater will be blood flow. So hereby, Siravyadha, interstitial pressure is

released, fresh blood rush towards the part, metabolic activity of the part is increased,

concurrently accumulated excessive pyruvic acid is drained. So the particular site may

be told where that dorsal venous arch is easily accessible.

In ‘Padaharsha’ – which is tingling and numbness commonly seen in

neuropathies due to various causes, where glucose uptake and glycolysis is impaired

due to various causes, presenting with tingling, numbness, pricking, burning etc. By

means of blood letting by phlebotomy there is increase in insulin sensitivity resulting

proper glucose uptake and glycolysis which can prevent degeneration of nerves by the

release of energy. So the phlebotomy done in said part i.e. two Angula above from

Kshipra Marma i.e. dorsal venous arch.

In ‘Chippa’, where it is the infection of nail bed of fingers causing redness,

tenderness, lymphangitis, formation of pus. By phlebotomy at dorsal venous arch,

venous drainage of the part and lymph drainage, where interstitial space pressure is

decreased facilitating migration of lymphocytes through vessel wall subsiding

infection, inflammation providing improvement in metabolism of cell.

In ‘Visarpa’, which is spreading lymphangitis or neuritis due to organisms or

viruses. The lesions starts as scratch and commences as rose pink rash which extends

to the skin in spreading nature. Vesicles appear sooner in the neck, face, upper limb

and lower limbs. By means of Siravyadha in two Angula above from Kshipra Marma

i.e. dorsal venous arch. Venous drainage of the part is improved. Blood rushed

towards the part, WBCs, macrophages coming towards the part to engulf the

infectious agents. So immediately inflammatory changes are neutralized as local

cellular metabolism is improved. And another mechanism is pressure in interstitial

fluid is decreased improving lymphatic circulation. By means of local blood letting

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directly bone marrow is stimulated to produce erythropoietin decreasing viraemia.

Reactivation of virus is stopped as WBCs are scattering towards the affected part. So

nerve inflammation may be reduced. So the particular site of Siravyadha may be

considered.

In ‘Vatarakta’, which is a metabolic disorder of impairment of purine

metabolism, serum uric acid level is high and also there is inadequate excretion i.e.

nothing but hyperurecaemia. The pathogenesis is unclear. Blood letting in dorsal

venous arch causes reduction in urea, uric acid. There is release of angiotensin

hormone which has got renal and adreno-cortical stimulatory effect providing

excretion of urea, uric acid by kidneys. That is why in gouty arthritis blood letting

done in site told by Sushruta.

In ‘Vatakantaka’ there is bony out growth usually extends from heal into the

soft tissue causing inflammation of plantar fascia and pain. That heel spur is

composed of calcium deposits. The osteoblasts secrete large quantity of alkaline

phosphate which is believed to increase local concentration of inorganic phosphates.

In such a way, they cause deposition of calcium salts. By doing phlebotomy in

recommended dorsal venous arch certain amount of alkaline phosphate is taken away

and also can be prevented by increased metabolism and blood flow. So the site of

Siravyadha may be accepted.

In ‘Vicharchika’ which is pruritc condition of skin. Because of predisposing

factors like chemicals, drugs irritations, large number of inflammatory cells cause

structural and functional integrity of epidermis resulting hyperplasia. Thickening

horny layer, formation of vesicles in epidermis. So there is erythema, crusting,

fissuring, oozing, pigmentation etc. by means of blood letting, blood is rushed and

provides oxygen and nutrients for proper growth of epidermis. The epinephrine and

nor-epinephrine hormones are released, acting as a anti-allergic. So the site of

Siravyadha may be considered.

In ‘Padadari’, fissure in sole due to scratching and infection i.e. nothing but

vertical loss of epidermis. Blood letting in dorsal venous arch will improve venous

drainage, concurrently local tissue metabolism is improved. Because of rush of blood

towards the part and proper drainage of metabolites and also release of hormones. So

the site can be considered.

In ‘Shleepada’, which is a condition where there is inflammation of lymphatic

vessels including mechanical blockage of lymphatic channels, resulting into

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lymphoedema. On the basis of physiology, venesection will help when blood is letted

out from the dorsal venous arch. So that the pressure in the interstitial fluid is reduced

concurrently pressure in the lymphatic channels is also reduced to provide relief of

blockage and opening of capillaries and also local cellular metabolism is improved.

The site four Angulas above from Gulpha Marma i.e. short saphenous vein is

considered.

In ‘Krostuka Sheersha’, which is an inflammatory involvement of joint due to

infectious agents like streptococci, staphylococci organisms where the predisposing

factors may be alcohol, drug abuse, immune suppressive therapy, causing synovitis.

Synovial swelling and also there is a release of condrolytic enzymes, contribute to

destruction of articular cartilage. By means of blood letting in long saphenous vein,

hyperurecaemia is reduced by the release of steroid hormones, effusion may be

resolved, fibrous adhesions are avoided. So the site of Siravyadha may be considered.

In ‘Khanja’, there is monoplegia, where there is incapability to walk. By

means of blood letting in four Angula above from Gulpha Sandhi done, because if

there is any thrombosis that will be dissolved by fibrinolytic activity of blood and also

there is removal of waste products, cellular metabolism is improved, various

hormones released to maintain homeostasis. So the site of Siravyadha dealt by

Sushruta may be considered.

In ‘Pangu’, there is cerebral palsy, which is ischemic necrosis in the brain to

reduce blood supply to neural tissue which is insufficient to meet the metabolic needs,

rapid fall in cerebral perfusion lead to diplegia. Cerebrum is most vascular area of the

brain. Metabolic factors have potent effect in controlling cerebral blood flow. They

are nothing but CO2, hydrogen, oxygen. An increase in CO2 or hydrogen ion

concentration increases cerebral blood flow, where as decrease in oxygen, that

increases the blood flow. By means of dilating cerebral blood vessels increase the

blood flow, which is inturn carries CO2 and acidic substances. Oxygen deficiency

increases the cerebral blood flow. On the basis of this theory, blood letting in long

saphenous may induce higher CO2 and hydrogen ion concentration which inturn cause

dilation of cerebral blood vessels, with increased blood flow, and also carrying acidic

substances from neural tissues.

In ‘Grudhrasi’, where there is pain along the sciatic nerve distribution, due to

lumbar disc diseases. Mechanical pressure on the nerve roots, the pain felt in the

buttocks, thigh, calf, paraesthesia along the nerve root and calf muscle weakness.

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There may be various stimuli like mechanical, chemical, thermal factors causing pain.

By means of blood letting in branch of great saphenous vein, four Angula above or

below from Janu Sandhi, blood flow to the compressed part may be increased by

angio-genesis. As aerobic metabolism is enhanced, the accumulation of lactic acid

may prevented and reduced. By means of blood letting hormones serotonin is released

which is believed to cause pre-synoptic and postsynoptic inhibition avoiding pain. So

if the pain is situated in back and thigh, the upper site is selected, if pain is radiated up

to the leg, lower site is selected.

In ‘Galaganda’, which is thyroid enlargement due to multiple factors. It may

be toxic or non-toxic, that is nothing but repeated and prolonged changes of

hyperplasia of thyroid tissue where there may be fibrosis. Blood letting in Uru-Mula

Sthita Sira which may directly stimulate pituitary and TSH and indirectly improve

metabolism of whole body by the release of numerous chemicals and hormones. As

the available veins of neck and abdomen are contraindicated for Siravyadha this site

might have been accepted for Siravyadha.

In ‘Pleehodara’, there is enlargement of spleen, due to various causes where

the spleen is heavy and firm. The capsule is tense and thick. By blood letting left

sided medial cubital vein, the reticuloendothelial cell of spleen rapidly remove debris,

bacteria, parasites. Usually reserved blood is ejected into the general circulation. The

fragile RBCs are washed off. Splenic vein is drained effectively. So blood letting

particularly on left sided medial cubital vein is considered.

In ‘Yakrutodara’, where there is enlargement of liver, due to various causes,

there may be fatty deposition of liver, or inflammation of hepatocytes or cirrhosis. By

means of blood letting in right sided medial cubitol vein reserved blood in the liver is

ejected into the general circulation, to cause decongestion. Epinephrine and nor-

epinephrine hormones are released, mobilizing fatty acids deposited in the liver.

Hepatocellular enzymatic activity is improved. Fresh RBCs are produced to utilize the

ferritin. By all these affects the enlargement of liver can be reduced. So the said site is

considered.

In ‘Kaphodara’, where there is accumulation of fat, so that an adipose tissue is

deposited. Blood letting in right medial vein helps to mobilize fatty acids. As they

help to improve the hepatocellular function by release of certain enzymes enhancing

fat metabolism. So that might be site of Siravyadha recommended.

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In ‘Kasa’ which is nothing but cough, as defense mechanism of body, in URI

and LRI or any infections of respiratory tract. When blood letting is done in right

sided medial cubital vein, the venous pressure in the right atrium may be decreased

resolving pulmonary congestion. So the site may be considered.

In ‘Shwasa’, the condition may be considered as breathlessness due to CCF or

emphysema or hyperurecaemia. By means of blood letting in right medial cubital

vein, the congestion of lung and liver is decreased. So the verdict of Sushruta can be

accepted.

In ‘Vishwachi’, that is injury to brachial plexus of the arm may mimic cervical

origin. It is nothing but brachial plexus neuritis. Locally by blood letting four Angula

above from Kurpara Sandhi i.e. basilic vein, the pain precipitating factors like lactic

acids are reduced. Blood supply to brachial plexus is improved, where there is aerobic

metabolism in the part. There is provision to release of hormone serotonin, which

inhibits pain of neuritis. In this way blood letting site may be considered.

In ‘Apachi’ which is an inflammatory condition of lymph nodes called

lymphadenitis. Lymph nodes undergo reactive changes in response to acute variety of

stimuli like infection, injury, neoplasia. They are firm, round swellings. By means of

blood letting venous drainage is improved, automatically lymphatic drainage is

improved, resolving in inflammation of lymph nodes by increased blood flow,

scattered WBCs, removal of waste products. So the part two Angula below from

Indrabasti Marma is selected.

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CONCLUSION

1. Sira means vein.

2. Veins are not only blood reservoirs, but having their own influence in blood

circulation and lymphatic circulation.

3. Lymphatic drainage is essential to maintain homeostasis.

4. Siravyadha is effective therapeutic tool in many health hazards if judiciously

administered.

5. The efficacy of Siravyadha is appreciated by ancient scholars and present day

modern peoples also.

6. Siravyadha is also beneficial in physiological maintenance of well-being.

7. The sites of Siravyadha told by Sushrutacharya are scientific and can be

adopted.

8. Irrespective of contraverises, the sites can be followed for Siravyadha.

9. Almost all the Siras told by Sushruta for Vyadhana purpose can be adopted in

clinical practice.

Recommendation for Future Study :

As the concept of Sira Shareera and Siravyadha Vidhi Shareera are still

unclear to grasp and adopt. So Shalya Tantra scholars can continue clinical study on

individual site of Siravyadha in individual diseases to evaluate therapeutic efficacy of

Siravyadha.

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SUMMARY

Ayurveda is as old as mankind, where the concepts have been evolved three

thousand years ago. It is the document where many Acharyas dedicatedly worked for

the benefit of mankind with the motive of welfare of human beings. On the contrary

the things are not properly passed onto the future generations. Because of this

generation gap, many concepts are unclear.

Regarding Rachana Shareera are concerned there are many technical terms

which are vague for a casual observer, teacher and students. So many lacunas may be

found in concepts of Rachana Shareera. Regarding above said dictum is concerned

there is very little information on ‘Sira Shareera’ and Siravyadha Vidhi Shareera’. So

here in present study comprehensive literary information is collected above the topics.

So regarding Sira Shareera with special reference to venous system is interpreted so

as to elicit meanings of the Sira, Dhamani and Srotas. An attempt has been made to

prove ‘Sira’ as ‘vein’ on literary grounds.

Regarding ‘Siravyadha Vidhi Shareera’ is concerned, it is effective Shodhana

therapy for letting of impure blood outside the body. As Basti is dominant line of

treatment in Kayachikitsa, Siravyadha is dominant line of treatment in Shalya Tantra.

Poorvakarma, Pradhanakarma and Paschatkarma are clearly explained on available

literary sources, because of Significance of Siravyadha is elicited on the basis of

classical references, modern information and internet. Modern people also appreciated

the effect of phlebotomy in various diseases.

The chief aim of the study is concerned it is anatomical location of Vedhya

Sirasthanas in particular diseases. This is clearly analyzed on anatomical,

physiological, patho-physiological grounds. As per Ayurvedic concepts and modern

concepts, an honest and logical interpretation is made to identify Siravyadhana

Sthanas in particular diseases, and have been critically analyzed. So as to fulfill the

objectives the discussions are made and conclusions are drawn and also future study

is recommended.

Page 155: Sandhigata siravyadha sr

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I

REFERENCES

1. srNit` (sri : .. (C S Su 30/12)

2. aS&Ü r±tvi(hn) (hri {(sri} . S&Ü r±tvi(hn) Fmn) . (Atharva 7/36/2)

3. S)ti: gi]y<y: (sri kfit` .. (Su. Sha. 7/18)

gi]y<: IAn³F: (sri Si)t: .. (A. H. Sha. 3/37)

4. kN<yi[d<S nisi. S¾dvi(hn)m[k]ki> p(rhr[t` . (Su. Sha. 7/23)

5. Äyip»vºRyIBti[ d[h> niIBt: p\sZti: (sri: . p\tini: p(Þn)kºdi(Úsid)ni> yYi jlm` .. (Su. Sha.

7/26)

6. as>d[SIAtti[ viy&: Si[P(yRvi>sRvºFnm` . (sriÆcik&öµy t#iAYi[ jnyRyvbh&km` ..(Su. Ni.

1/32)

7. Fit*ni> p*rN> vN< ApS<Xinms>>Sym`. Avi: (sri: s>yrd|±t> k&Áyi<µciºyin`

g&Nin(p.. (Su. Sha. 7/15)

8. tisi> niIBm*<l> ttÅc p\sr>(t U¹v<mFIAty<k` ..

yivRyAt& (sri: kiy< s>BvIºt Sr)(rNim` . ni¿yi> svi<> (nbÜiAti: p\tºvIºt smºtt: .. niIBAYi: p\iINni> p\iN: p\iNin` ni(BÄy&piI~ti:

. (sriIBvZti niIBÅck|iniIB(rvirk]: .. (Su Sha 7/3-5)

9. dS m*l(Sri ñRAYiAti: sv<> sv<ti[ vp&: . rsiRmk> vhºRyi[jAt(ÒibÜ> (h c[IOTtm` .. AY*lm*li: s&s*ZÈmig\i: p#ir[Kip\tinvt` .. IBwºt[ tiAtt: sßStiºyisi> BvIºt t& . (A H Sha 3/18-

19)

10. sIºF bºFn ki(r·yi[ di[P Fit&vhi (sri: .

Page 156: Sandhigata siravyadha sr

References

II

ni¿yi> svi< (nbÜiAti: p\tºvIºt smºvt: .. (Bha Pra

3/244)

11. t#ii@Ni vitvhi: p*y<ºt[ viy&ni (sri: . (p_iid&ONiÆc n)liÆc S)ti gi]y<: IAYri: kfit``

. asZ³vhiAt& ri[Ih·y: (sri niRy&ON S)tli: .. (Su.

Sha. 7/18)

12. sß (sriSti(n BvIºt . yi(B(rd> Sr)rmirim ev jlhi(rN)IB:. k[dir ev c k&Ãyi(B@pIéHt[¥n&gZHt[ cik&ønp\sirNi(d(B(v<S[[P]:

d\&mp#is[vÒi(mv tisi> p\tini: tisi> niIBm<*l> ttá

p\srºRy*¹v<mFIAty<k` c .. (Su. Sha. 7 /13) 13. t#i Åyivi@Ni: s*Èmi: p*Ni<(räi: xNiIRsri: ..

p\ApIºdºyá vitis\> vhºt[ (p_iSi[INtm` . ApSi<[ONi: S)G\vi(hºyi[ n)lp)ti: kf> p&n: .. gi]y<: Ié³Fi: IAYri: S)ti: s>sZOT> (l©s§r[ g*Qi: smIAYti: Ié³Fi ri[(h·y: S&ÜSi[(Ntm` .. (A.S. Sha. 6/8)

14. a#i p\Ni(l(B: k&ÃyiIB(r(t dZOTiºtÚy> AY*ls*Èm IsriB[dit` .. (Bha. Pra. 3/ 245)

15. Ik|yiNi> ap\(tGitmmi[h> vZIÛkm<Nim` . kri[Ryºyin` g&Ni>ái(p Avi: (sri: pvnárn` .. (Su.

Sha. 7/9)

16. Ik|yiNi> ap\(tGitmmi[h> vZIÛkm<Nim` . kri[Ryºyin` g&Ni>ái(p Avi: (sri: pvnárn` .. (Su.

Sha. 7/9) 17. ydi t& k&Ipti[ viy&: Avi: (sri: p\(tpwt[ .

Page 157: Sandhigata siravyadha sr

References

III

tdi¥Ay IvIvFi ri[gi jiyºt[ vits>Bvi: .. (Su. Sha. 7/9)

18. B|i(jON&timºn@(cmI³n d)I¼tmri[gtim` . s>sp<n` Avi: Isri: Ip_i> k&yi<Ëiºn` g&Nin(p

.. (Su. Sha. 7/10)\

19. ydi t& k&Ipt> Ip_i> s[vn[ Avivhi: (sri:. tdi¥Ay IvIvFi ri[gi jiyºt[ Ip_is>Bvi: .. (Su. Sha.

7/11)

20. An[hm©[P& sIºFni> AY]y<> blm&d)Ni<nim` ..

kri[Ryºyin` g&Ni>ái(p blis: Avi: (sriárn` .. (Su.

Sha. 7/12)

21. ydi t& k&Ipt: Ål[Omi Avi: (sri: p\(tpwt[ . tdi¥Ay IvIvFi ri[gi jiyºt[ Ål[Oms>Bvi: .. (Su. Sha.

7/13)

22. Fit*ni> p*rN> kiy<> ApS<Xinms>Sym` . Avi: Isri: s>crd\±t> k&yi<µc aºyin` g&NinIp

.. (Su. Sha. 7/14)

23. ydi t& k&Ipt> r±t s[vt[r±tvhi: (sri:. tdi¥Ay IvIvFi ri[gi jiyºt[ r±ts>Bvi: .. (Su. Sha.

7/15) >24. n (h vit> (sri: kiIáÒi (p_i> k[vl> tYi .

Ål[OmiN> vi vh>Rºti at: sv<vhi: AmZti .. p\d&OTini> (h di[PiNi> m*IµC<tini Fivtim` . F\&vmºmig<gmnmt: sv<vhi: AmZti: .. (Su.

Sha. 7/16-17)

25. tisi> m*lIsiriÅcRvi(r>St`: tisi> vitvi(hºyi[ dS Ip_ivi(hºyi[ dS,

kfvi(hºyi[ dS dSr±tvi(hºy: . tisi> t& vitvi(hºyini> vitAYingtini>

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References

IV

pöcs¼t(tSt> Bv>It tiviRy Ip_ivi(hºy: Ip_iAYin[,kfvi(hºyá kfAYin[,

r±tvi(hºyá ykZt¼l)ði[: Evm[ti(n s¼tIsriSti(n Bv>(t .. (Su. Sha. 7/6) 26. dSm*lIsri ñdyp\(tbÛi: svi<>©p\Ry©[Ovi[ji[ nyIºt tRp\(tbÛi Sr)rc[OTi: .

tiAt& Úvy>g&l> a©&lmFi<©&l> yv> yviF<> c gRvi d\&mp#i s[vn)p\tinv(Ûwmini: s¼tSti(n BvIºt .. (A. S. Sha. 6/2)

27. tisi> yYiAv> t&yi<>S(vBig[n pöcs¼tIºFk> Xitm(nlr±t> vh(t .

EP (vBig: (p_iÅl[Om S&Úr±t[Ov(p . IAYti H[v> d[hnm&gZh`Ni(t di[[Pi: s. ÄyRy[n t& p)Dy(ºt .. (A. S. Sha. 6/7)

28. t#i vitvi(hºy: (sri EkIAmn` sI±¸n pöc(v>S(t:, Et[n[trs(±Y bih& c Äyi²yiti]. (vS[PAt& ki[OT[ ct&IAS>t` tisi> g&dm[QiI~ti: ~i[·yiOTmi] o[ o[ piÅv<yi[: PT` pZOT[ tivºy[ Ev ci[dr[ dS vxIs . (Su Sha. 7/7)

29. tisi> ct&:St) SiKis& . t#i Pi[DSÄyi(Fn)yi: PT`I#i>S> StmºtSCi] t#i

oi(#iS<t` . ct&OPOT`y(Fk> Stm*¹v<> t#ii(p pöcSt` ..

(A.S. Sha. 6/13)

30. ñdi[ rsi[ In:sr(t tAmid[(t c sv<S: . (sri(Bñ<dy> v](t tAmit` p\Bvi: (sri: .. (Bhe. Sam.

Su. 20/3)

31. dS Fmºyi[ ñdy[ (nbÛi BvIºt . ti: p\Bv[ ct&r>g&lmi#i> gRvi (v>S(tB<v<(t . Evm[ti dS Fmºy: PIOTB<v>(t .

Page 159: Sandhigata siravyadha sr

References

V

t#i t& Bv>It #)IN Stshs|iIN PIOT(ry> jili(n (sriNim` .(Bhe.Sam. Su. 4/27) 32. twYi – vZx: SiKivZt: fmpliS]Ktr(t sv<#i .

twYi vihºyi[¥Åm(BKtt: tYiy> (sriIBrvtt: . ri[mk*p[ ri[mk*p[ MAy (srim&K> Bv(t, yt: Av[d: xrt)(t .. (Bhe. Sam. Su. 4/27)

33. at U´v<> p\vxiIm n (v´y[wi: Isri IBPk` . v]kÃy> mrN> ci(p ÄyFi_iisi> F\v> Bv[t` .. IsriSti(n cRvi(r (vwiµCiSiKis& b&IÛmin` . PT`I#i>Söc St> ki[Oq[ ct&:POT> c m*F<In .. SiKis& Pi[DS Isri: ki[Oq[ oi(#i>Sd[v t& . pøiS÷#i&Ni> c u¹v<mÄy¹yi: p(rk)It<ti: ..(Su

Sha. 19-21)

34. t#i (sriStm[kIAmn` sI±Y Bv(t tisi> jilFri Rv[ki (ts|ái¿yºri: t#ii[v)<s>X[ o[ li[(htix s>Xi c]ki tiARvÄy¹yi: .. (Su. Sha. 7/23)

35. y(dr[d` b(hdi[<Pin` pöcdi S[Fn> c tt` . (n$hi[ vmn> kiy(Sri[r[ki[ as\(vsZ(t .. (A. H. Su.

14/5)

36. d[hAy @(Fr> m*l> @IFr[N]v Fiy<t[ . tAmit` yRn[n s>rÈy r±t> j)v e(t IAY(t : . (Su.

Su. 14/44)

37. t#i SAt\(vs\ivN> Io(vF> p\Cºn> (sriÄFn> c . (Su. Su. 14/24)

38. aSAt\·y[v SAt\kiy< k&v<Iºt an&SAt\iIN .. (Su.

Su. 8/13)

39. t#i piddihpidhP<(c¼p(vsp< vitSi[INt vitk·Tk (vc(c<kipiddir)p\BZ(tP& Ixp\mm<N up(rOTid` oy>g&l[ v\)(hm&K[n (sri> (v¹y[t`

Page 160: Sandhigata siravyadha sr

References

VI

Ål)pd[ tIµc(kIRst[ . yYi vÈyt[ k|i[Oq&k(Sr: Köjp©&lvitv[dnis& j>Giyi> g&ÃfAyi[p(r ct&r©&l[, apµyi(mºd\bAt[rFiAtid` oy>©&l[, jin&sºF[@py<Fip vi ct&r©&l[ gZF\Ayi>, U@m*ls>I~ti> glg·D[, Et[n[trsI±Y bih* c Äyi²yiti]; (vS[PAt& vimbihi] k*p<rsºF[r¿y>rti[------ISri[ri[g(FmºYp\BZ(tP& ri[g[IOv(t .. (Su. Su.

8/17)

40. bilAY(vr$xxtx)NB)@p(r~i>ºt mwpi¹vAt\) k(S<t v(mt(v(r±ti¥AYi(pt an&vi(st jig(rt ±l)bkZSgIB<N)ni> kisÅvisSi[Pp\vZܶvrix[pk pxiGiti[pvis (ppisim*µCi< p\p)(Dtini> c (sri> n (v¹y[t`, yiÅciÄyi¹yi: Äyi¹yiÅcidZOTi dZOTiÅciIº#iti:, yIº#itiÅcin&IRYti eIt .. (Su. Sha. 8/3)

41. n]vi(tS)t[ niRy&ON[ n p\vit[ n ciIB\t[ . (sriNi> ÄyFn> kiy<mri[g[ vi kdicn .. (Su. Sha.

8.7)

42. ÄyB\[ vPi<s& (v¹y[_i& g\)Omkil[ t& S)tl[ . h[mºt[ m¹yið[ SAt\kiliAt\\y: AmZti : (Su. Sha.

8/10)

43. aY kZtAvARyynmit&r> ÄyiIFblisiRÀyiwp[Èy IAn³F ji©l>rs> yvig&> c piyIyRvi m&h*t<mi#imiÅvi(st> p*vi<ð[¥prð[ -------k*p<r smIAtpid> p\Ry(dRym&pv[Åy[t` . (A.

H. Su. 27/18)

44. bIlni[ bh&di[PAy vy: AYAy: Sr)(rN: . pr> p\miNImµCIºt p\AY> Si[INtmi[xN[ .. (Su.

Sha. 8/16)

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45. d&OTÄyFi (v>S(t: - d&Iv<Üi¥(t(vÜi k&(øti Ipµcti k&IÍti¥p\s\&ti¥Ry&d)Ni<¥ºt[[ (vÜip(rS&Oki k*INti v(pti¥tin&IRYt(r¹yi SAt\htiIty<I³vÜi(v¹yi (vd\&ti F[n&ki p&n: p&n(v<¹yi (sriAniÂvIAYsIºFmm<s& µy[(t .(Su. Sha. 8./18)

46. (sriÄFiIÅc(kRsiF<> SÃytº#i[ p\k)It<t: yYi p\iIN(ht: sÀy³bIAt: kiyIc(kIRst[ .. (Su. Sha.

8/23)

47. (sriÄFIÅc(kRsiF<> sÀp*N< vi Ic(kIRstm` . SÃytº#i[ AmZZti[ yd` bIAt: kiyIc(kIRst[ ..

yYi r±tm(FOTin> IvkiriNi> Ivk(rNim` . anºy (h tYi d\Äy> km<[d> p\Ym> tt: .. (A. Sam.

Su. 36/4-5)

48. p\sºn> vN[<Iºd\yImIºd\yiYi<n` eµCºtmÄywin` s&KiIºvti t&IOT bili[pºn> (vS&Ü r±t p&@P vd>(t .. (Cha. Su. 24/24)

49. An[hi(dIB: (k|yiiyi[g]n< tYi l[pn]r(p. yiºRyiS& ÄyiFy: SiIºt: yYi sÀyk` (sriÄyFit` ..

(Su. Sha. 8/22)

50. Rv³di[P g\ºYy: Si[fi: ri[gi: Si[INtjiÅc y[ . r±tmi[xNSi<lini> n Bv>(t kdicn .. (Su. Su. 14/34)

51. t#i piddihpidhP<(c¼p(vsp< vitSi[INt vitk·Tk (vcIc<ki piddir) p\BZ(tP& Ixp\mmi<IN up(rOTid` H©&l[ v|)h)m&K[n (sri> (v¹y[t` .. (Su. Sha. 8/17)

52. pidyi[: k&@t[ dih> Ip_iis<k`s(hti[¥(nl:. (vS[PtÆc¦k\mNit` piddih> tmi(dS[t`` .. (Su. Ni.

1/80)

53. ñOytÅcirNi]] yAy BvtÅc p|s&¼tvt` . pidhP<: s (vX[y: kfvitp\ki[pj: .. (Su. Ni. 1/31)

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54. nKmi>smIFOTiy Ip_i> vitÆc v[dnim` . kri[(t dihpiki[ c t> ÄyiIF> Ic¼pmiIdS[t` .. (Su.

Ni. 13/19)

55. k&y<t[ Ip_ii(nl> pik> nKmi>s@ji> Ic¼pmxtri[g c (vwid&pn> nK> c tm` . (A. S. Ut. 36/5)

56. Rv§mi>sSi[INtgti: k&IptiAt& di[Pi: . svi<©si(rNiImhiIAYtmiRmIl©m` .. k&v<Iºt IvAtZtmn&ºntmiS& Si[f> t> sv<ti> IvsrNiµc (vsp<mih&: ..

(Su. Ni. 10/3)

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IX

57. r±t> lIski Rv¦`mis> d*Oy> di[PiA#iyi[ mli: .

Ivsp<Ni> sm&Rp_ii] IvX[yi: s¼t Fitv: .. (Ca.

Chi. 21/15)

58. vitr±t> Ih d&OT[n r±t[n c (vISOTs>p|iI¼tk> (vkiriºtrm[v ..

p|iyS: s&k&miriNi> Im¸yihiri(vhi(rNim`. Si[kiÅc p|mdimwÄyiyimiÅciItp)Dnit` .. ât&siRÀy(vpyi<sit` An[hid)ni> c IvB|mit` . aÄyviy< tYi AY*l[ vitr±t> p|k&¼yIt .. (Su. Ni.

1/40-41)

59. Ixp|> r±t> d&IOTmiyiIt tµc viyi[mi<g> s>@Nd`¹yiS& yit: k|&Ûi[¥RyY<> migi<ri[Fit` s viy&rRy&Id\±t> d&Py[d\±tmiS& .. tt` s>pZ±t> viy&ni d&IPt[n tTp\ibÃyid&µyt[ vitr±tm` . tÚt` Ip_i> d*IPt[nisZji¥ä Ål[Omi d&OTi[ d*IPt[nisZji¥ä .. (Su. Ni. 1/43-44)

60. ºyAt[ t& (vPmpid[ @j: k&yi<t` sm)rN: . vitk·Tk: eRy[P: (vX[y: K&DIlkiI~t: .. (Su. Ni.

1/76)

61. ri¶yi[¥(tk·D`vIt@j: s@ji BvIºt gi#i[P& IvcIc<kiyim` .. (Su. Ni. 5/13)

62. P(rk|mNS)lAy viy&rRyY<$xyi[: . Pidyi[: k@t[ dir)> s@ji> tls>I~t: .. (Su. Ni. 13/28)

63. An[hAv[di[pºn[t& Ål)pd[¥Inlj[ (BPk` . kZRvi g&Ãfi[p(r Isri> (v¹y[_i& ct&r©&l[ .. (Su.

Chi. 19/52)

64. g&ÃfAyiF: Isri> (v¹y[t` Ål)pd[ Ip_is>Bv[ .

Page 164: Sandhigata siravyadha sr

References

X

Ip_i>G»)> c (k|yi> k&yi<t` Ip_iib<&d(vsp<vt` .. (Su. Chi. 19/55)

65. (sri> s&Iv(dti> (v¹y[d¦`g&Oq[ Ål]IOmk[ IBPk` .. (Su. Chi. 19/56)

66. p&riN[ udkB*IyOTi: sv<t&<P& c S)tli: . y[ d[SiAt[P& jiy>t[ Ål)pdi(n (vS[Pt: .. (Su. Ni.

12/17)

67. k&(ptiAt& di[Pi vit(p_iÅl[OmiNi[¥F p|pºn: v«Ni[@ jin&jªis& avIt¹ymini: kiliºtr[N pidmi(~Ry Sn]: Si[f> jnyIºt tt` Ål)pd> eRyicxt[ .. (Su. Ni. 12/13)

68. k|i[OT&kISr: Köjp©&l:vitv[dnis& jªiyi> g&ÃfAyi[p(r ct&r©&l[ .. (Su. Sha. 8/17)

69. vitSi[(Ntj: Si[fi[ jin&m¹y[mhi@j: . (Sr: k|i[OT&kp*v<> t& AY*l:

k|i[OT&km*F<vt` .. (Su. Ni. 1/76)

70. viy& kT`yi IAYt: sºkY: k·DrimiIxp[wydi .

KöjAtdi Bv[¶jºt&: p©&: sºkYi[oyi[v<Fit` .. (Su.

Ni. 1/77)

71. viy& kT`yi IAYt: sºkY: k·DrimiIxp[wydi . KöjAtdi Bv[¶jºt&: p©&: sºkYi[oyi[v<Fit` .. (Su.

Ni. 1/77)

72. apµyiImºd|bAt[rFAtid` o©&l[ . (Su. Ni. 11/10)

73. Jin&sºF[@py<Fi[ vi ct&r©&l[ gZF|Ayim` . (Su. Sha. 8/17)

74. PiION<p|RyI©&(lni> t& k·Dri yi¥(nli(d<ti sk`¸n: x[p> IngZh`N)yid` gZF|s)It (h si

AmZti .. (Su. Ni. 1/74)

75. IAfk`p*vi< kITpZOTi[@jin&j>Gipid> k|mit` .

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XI

gZF|s) AÀB@k`ti[d]gZh`Ni(t Ap>dt[ m&h&: ..

vitit` kfit` tºd|igi]rviri[ckiIºvti . (Cha. Chi. 28/56)

76. U@m*ls>I~tini> glg·D[ Et[n[ntrsI±Y bihv Äyi²yiti] : .(Su. Sha. 8/17)

77. vit: kfÅc[v gl[ p\vZÜi[ mºy[ t& s>sZ¶y tY]v m[d: . k&v<>(t g·D> k|mS: AvIl©]: smIºvt> t> glg·Dmih& : .. (Su. Ni. 12/23)

78. (vS[PAt& vimbihi] k*p<rs>F[r¿yºtrti[ bih&m¹y[ ¼l)(ð k(nIOTki aniImkyi[m<¹y[ vi ..(Su. Sha. 8/17)

79. IvdHIBOyIºdrtAy jºti[: p\d&OTmRyY<msZk` kfÅc .

¼l)hiIBvZIÜ> stt> kri[(t ¼l)hi[dr> tt` p\vd>(t t¶zi: ..

vim[ c piÆv<> vZIÜm[(t (vS[Ptis)d(t cit&ri[¥#i .(Su. Ni. 7/14-15)

80. Ev> dIxN bihi] ykZd`diÃy[ Etim[v c kisÅvisyi[r·yi(dSIºt ..

(Su. Sha. 8/17)

81. p|iNi[ Hy&dinin&gt: p\d&OT: s>IBºnki>AyAvnt&ÃyGi[P : .

Inr[It vk|#iit` shsi sdi[Pi[ mInIPIB: kis eIt p|IdOT: .. (Su. Ut. 52/5)

82. tl> p|Ry>g&l)ni> t& k·Dri bih&pZOTt: biói[: km<xykr) (vÅvic) (h si AmZti .. (Su. Ni.

1/75)

83. gZF\Ayi>Imv (vÅviµyi> .. (Su. Sha. 8/17)

Page 166: Sandhigata siravyadha sr

Bibliography

VIII

BIBLIOGRAPHY

01. Sharma Tarachand : Ayurvediya Sharira Rachana Vijnana, First Edition,

Rohtak ; Nath Pustak Bhandar, Railway Road, 1983, 8th Chapter, p 214.

02. Sahitya Vidwan Chakravarti Shrinivasa Gopalacharya (Edi): Shabdartha

Kausthubha, Sanskrit to Kannada Shabda Kosha, VI part, Bangalore, 1987, p

51.

03. Shastri Kashinath, Chaturvedi Gorakhnath : Caraka Samhita, Sutrasthana

with Vidyotinie Hindi commentary, II Edition, Varanasi, Chaukhambha

Bharati Academy, P B No. 1065, Gopal Mandir Lane, 1998, p 584.

04. Govind Raju U : Human Anatomy in Ayurveda, 1st Edition, Bidar, Sri

Publications, Basava Nagar, Feb 2004, 7th Chapter, p 63.

05. Sharma Tarachand : Ayurvediya Sharira Rachana Vijnana, First Edition,

Rohtak ; Nath Pustak Bhandar, Railway Road, 1983, 8th Chapter, p 214.

06. Ibid

07. Ibid

08. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

Academy, Gopal Mandir Lane, 1997, p 61.

09. Ibid

10. Ibid

11. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

Academy, Gopal Mandir Lane, 1997, p 235.

12. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

Academy, Gopal Mandir Lane, 1997, p 61.

13. Sharma P. V. : Sushruta Samhita, Vol. II, I Edition, Varanasi ;Chaukhambha

Vishvabharathi, 2000, pp 200.

14. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata, Vol. I, First edition,

Varanasi ;Chaukhambha Vishvabharathi, 1991, pp 56.

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15. Mishra Bramashankara, Vaisya Rupalalji : Bhavaprakasha of

Bhavamishra including Nighantu part, Vol. I, 10th Edition, Varanasi;

Chaukhambha Publications, 2002, p 244.

16. Shrikantha Murthy K.R : Sushruta Samhita Vol.II, I Edition, Varanasi

Chaukhambha Orientalia, P. B. No. 1032, Gokul Bhavan, Gopal Mandir Lane,

2001, p 125.

17. Thatte D. G. :Sushruta Samhita of Sushruta, Vol. III, I Edition, with English

translation, Varanasi; Chaukhambha Orientalia, P B No. 1032, , 1994, p 143.

18. Srikantha Murthy K. R : Astanga Samgraha of Vagbhata, Vol.II, 5th Edition;

Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal

Mandir Lane, 2005, p 78.

19. Mishra Bramashankara, Vaisya Rupalalji : Bhavaprakasha of

Bhavamishra including Nighantu part, Vol. I, 10th Edition, Varanasi;

Chaukhambha Publications, 2002, p 76.

20. Thatte D. G. :Sushruta Samhita of Sushruta, Vol. III, I Edition, with English

translation, Varanasi; Chaukhambha Orientalia, P B No. 1032, , 1994, p 143.

21. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

Academy, Gopal Mandir Lane, 1997, p 60.

22. Ibid

23. Ibid

24. Ibid

25. Ibid

26. Ibid

27. Ibid

28. Ibid

29. Thatte D. G. :Sushruta Samhita of Sushruta, Vol. III, I Edition, with English

translation, Varanasi; Chaukhambha Orientalia, P B No. 1032, , 1994, p 140.

30. Ibid

31. Srikantha Murthy K. R : Astanga Samgraha of Vagbhata, Vol.II, 5th Edition;

Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal

Mandir Lane, 2005, p 77.

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32. Srikantha Murthy K. R : Astanga Samgraha of Vagbhata, Vol.II, 5th Edition;

Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal

Mandir Lane, 2005, p 68.

33. Srikantha Murthy K. R : Astanga Samgraha of Vagbhata, Vol.II, 5th Edition;

Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal

Mandir Lane, 2005, p 77.

34. Srikantha Murthy K. R : Astanga Samgraha of Vagbhata, Vol.II, 5th Edition;

Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal

Mandir Lane, 2005, p 76.

35. Ibid

36. Krishna Murthy K. H : Bhela Samhita with English translation and critical

notes, I edition, Varanasi ; Chaukhambha Vishwabharati, 2000, p 88.

37. Ibid

38. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

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39. Ibid

40. Saraswathi Gananath Sen : Sanjnapancha Vimarsha, Varanasi; Krishna Das

Academy, 1993, pp 54-70.

41. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata with text, English

translation, etc, Vol. I, third edition, Varanasi ;Krishnadas Academy, Oriental

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42. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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43. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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45. Ibid p 29.

46. Ibid p 43.

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47. Ibid p 68.

48. Ibid p 43.

49. Ibid p 49.

50. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata with text, English

translation, etc, Vol. I, third edition, Varanasi ;Krishnadas Academy, Oriental

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51. Atridev : Ayurveda Brihat Itihas, Varanasi ; Chaukhambha Sanskrit

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52. Sharma P V : Ayurveda Vaigyanik Itihas, first edition, Varanasi ;

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53. Ritchie A. C : Boyd’s textbook of pathology, Vol. I, 8th edition, 1970, pp

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55. Ibid p 65.

56. Ibid p 64.

57. Ibid p 63.

58. Ibid

59. Ibid p 64.

60. Ibid p 65.

61. Ibid p 54.

62. Ibid p 65.

63. Ibid

64. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata with text, English

translation, etc, Vol. I, third edition, Varanasi ;Krishnadas Academy, Oriental

Publishers and Distributor, P. B. No. 1118, Gopal Mandir Lane, 1996, pp 192.

65. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

Sandipika Hindi commentary, 11th edition, Varanasi; Chaukhambha Bharati

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66. Tripathi Ravidutt : Astanga Samgraha, Sutra Sthana of Vagbhata, Delhi ;

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69. Ibid p 54.

70. Ibid p 103

71. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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72. Lele Avinash, Ranade Subash, Frawley David : The most secrets of

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50.

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74. Thatte D. G. :Sushruta Samhita of Sushruta, Vol. III, I Edition, with English

translation, Varanasi; Chaukhambha Orientalia, P B No. 1032, , 1994, p 158.

75. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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76. Sainani Gurumukh S : A P I T B of medicine, 6th edition, Mumbai ; National

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77. Guyton Arthur C, Hall John E : Textbook of Medical Physiology, 9th

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Harcourt Brace and company, Independence Square West, Philadelphia, 1996,

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84. Shastri Kashinath, Chaturvedi Gorakhnath : Caraka Samhita, Sutrasthana

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86. Russel R. C. G, Williams N. S., Balstrode C. J. K. : Bailey and Love’s Short

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87. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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88. Ibid p 129.

89. Guyton Arthur C, Hall John E : Textbook of Medical Physiology, 9th

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91. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata, Vol. II, Second

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92. Harsh Mohan : Textbook of Pathology, 5th edition, New Delhi : Jaypee

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95. Sainani Gurumukh S : A P I Textbook of medicine, 6th edition, Mumbai ;

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96. Shastri Ambikadatta : Sushruta Samhita of Sushruta with Ayurveda Tattva

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100. Ibid p 280.

101. Sainani Gurumukh S : A P I Textbook of medicine, 6th edition, Mumbai ;

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103. Lele Avinash, Ranade Subash, Frawley David : The most secrets of

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106. Harsh Mohan : Textbook of Pathology, 5th edition, New Delhi : Jaypee

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