Scott Austin - Frog Heart Lab Report - Section A07 · ! 1!...
Transcript of Scott Austin - Frog Heart Lab Report - Section A07 · ! 1!...
1
Introduction:
The heart muscle is unlike other organs in the body, powered electrically and on it’s
own. It is completely capable of function without neuronal input. When removed from the
body, the heart is capable of contraction when supplied with necessary nutrients (Faller,
2004, p. 214).
Contractile and autorhythmic cells are the two main cell types within the heart.
99% of the total cells in the human heart are contractile cells. These cells are responsible
for pumping blood by contracting the heart. Autorhythmic cells comprise the remainder of
cells in the heart, and are responsible for initiating and conducting action potentials within
the heart (Sherwood, 2010, p. 309).
Autorhythmic cells have no resting potential. Instead, they slowly depolarize until
threshold is reached, then fire an action potential. This is known as pacemaker activity
(Sherwood, 2010, p. 309). The spread of an action potential from the autorhythmic cell to
the contractile cell leads to the beating observed in the heart.
Ionic movement of Na+ through hyperpolarization of specific voltage gated channels
is the initial source of the action potential in the autorhythmic cell. K+ channels and Ca2+
channels additionally contribute to the pacemaker potential in the cell. These ionic shifts
result in the pacemaker activity of the heart (Sherwood, 2010, p. 310).
In the bullfrog, autorhythmic cells are found primarily in the sinus venosus. This is
the primary pacemaker in the frog heart. From the primary pacemaker an action potential
is able to spread to contractile cells via gap junctions (Sherwood, 2010, p. 308).
Contractile cells maintain a steadier resting potential than the autorhythmic cells.
This is mainly due to leaky K+ channels, which keep the membrane potential close to the K+
2
equilibrium potential. The action potential looks markedly different in a contractile cell
than in an autorhythmic cell. The contractile cell contains fast Na+ channels providing a
rapid influx of Na+; transient K+ channels leading to a brief repolarization period; L-‐type
Ca2+ channels, which are much slower than it’s T-‐type counterpart, leading to a plateau
period; and a rapid efflux of K+ via voltage gated K+ channels (Sherwood, 2010, p. 314).
Both the parasympathetic and the sympathetic nervous system innervate the heart,
having opposing effects on heart rate and strength of contraction (Sherwood, 2010, p. 325).
The parasympathetic nerve in the heart is the Vagus nerve and releases acetylcholine to
bind with muscarinic receptors leading to a decrease in rate of depolarization and a
decrease in heart rate. Over stimulating the Vagus nerve can lead to bradycardia leading to
cardiac arrest. The sympathetic nervous system releases norepinephrine to bind with β-‐
adrenergic receptors leading to an increased rate of depolarization and an increase in heart
rate (Sherwood, 2010, p. 326).
Cardiac output is determined by heart rate and stroke volume. Stroke volume is
controlled by intrinsic and extrinsic controls. Intrinsic control is based on how much blood
returns to the heart and how much blood is pumped out. This is the Frank-‐Starling law of
the heart. The more filling that takes place, the more force that blood is ejected with.
Larger venous return equals larger stroke volume (Sherwood, 2010, p. 328). Extrinsic
controls in the heart are a result of sympathetic stimulation. Sympathetic stimulation
releases norepinephrine and epinephrine, leading to increased cytosolic Ca2+, which leads
to increased contractile force resulting in increased cardiac output (Sherwood, 2010, p.
329).
3
Methods:
The procedure followed for the lab can be found in the NPB 101L Physiology Lab
Manual (Bautista & Korber, 2009, p. 54). Prior to the experiment the bullfrog was double
pithed by the lab TA’s. The brain and spinal cord were destroyed so the frog could not feel
pain or control its own movement. The frog was kept moist with a paper towel dampened
with deionized water. Once the heart was exposed the tissue was fed nutrients through
application of Ringers saline solution. Ringers solution is rich in electrolyte ions Ca2+, Na+,
and K+.
The abdomen was opened avoiding veins. The pectoral girdle was cut through. The
pericardium was removed and the heart was exposed. The Vagus nerve was isolated and
confirmed through stimulation and observation of bradycardia.
The force transducer was calibrated as per lab manual instruction and the ventricle
was punctured with wire ensuring un-‐insulated areas were in contact with the tissue and
the end of the wire at the force transducer. The left leg of the bullfrog was punctured with
a T-‐pin and ground wires were connected to the T-‐pin.
All experiments were performed as presented in the lab manual. Deviations from
the lab manual occurred in Part 4: Extrasystolic Contractions. For the early diastole
experiment only 1 extrasystole was recorded. Additionally in Part 6: Effects of
Epinephrine, the frog heart was injected three times with epinephrine and data were
collected for 3 minutes post injection.
4
Results:
Part 3: Electrical & Mechanical Activity of the Heart
With a starting baseline tension of 0.0-‐0.1g, average arterial contraction force was
measured. Atrial contractions were analyzed every 15 seconds for 2 minutes utilizing
maximum tension in a P wave (Figure 1).
Figure 1: The tension (g) at 15-‐second intervals over a 2-‐minute duration during atrial contraction in the
bullfrog’s heart represented in the blue line averaged 0.38g. Contraction force initially increased then
decreased, evening out over the data sample. Baseline tension was 0.0-‐0.1g. Time is measured in seconds
along the X-‐axis, and contraction force is measured in grams along the Y-‐axis.
Ventricular contraction force was established by analyzing maximum tension over a
2 minute period every 15 seconds (Figure 2).
0.3
0.35
0.4
0.45
0 15 30 45 60 75 90 105 120
Contraction Force
(grams)
Time (seconds)
Atrial Contraction Force
Measured Tension
5
Figure 2: The tension (g) at 15-‐second intervals over a 2-‐minute duration during atrial contraction in the
bullfrog’s heart represented in the blue line averaged 1.35g. Baseline tension was 0.0-‐0.1g. Force of
contraction declined over the data sample. Time is measured in seconds along the X-‐axis, and contraction
force is measured in grams along the Y-‐axis.
The average heart rate of 38.95 BPM was analyzed measuring the beginning of
contractile phase 1 of the electrical signal of contraction to the same point of the next
electrical signal (Figure 3).
Figure 3: The beats per minute (BPM) at 15-‐second intervals for a 2-‐minute period represented by the blue
line averaged 38.95 BPM. There was an initial increase in BPM, peaking at 40.81, a gradual decrease, finally
increasing. Time is measured in seconds along the X-‐axis, and beats per minute (BPM) are measured along
the Y-‐axis.
The average latency between mechanical and electrical activity was analyzed
measuring from the beginning of phase 0 of the contraction cycle of the electrical activity to
the beginning of ventricular contraction and was calculated to be an average of 0.30
1.2
1.3
1.4
1.5
0 15 30 45 60 75 90 105 120
Contraction Force
(grams)
Time (seconds)
Ventricular Contraction Force
Measured Tension
37
38
39
40
41
0 15 30 45 60 75 90 105 120
Beats Per Minute
(BPM
)
Time (seconds)
Heart Rate (BPM)
Beats Per Minute (BPM)
6
seconds. The measurements taken at 15-‐second intervals over a 2-‐minute time period as
compared to the average baseline latency of 0.30 seconds from phase 0 of the electrical
contraction cycle to the start of mechanical contraction (Figure 4).
Figure 4: The latency between the onset of electrical activity (phase 0) and the initiation of ventricular
contraction was averaged to be 0.30 seconds. Individual measurements were taken every 15-‐seconds over a
2-‐minute time period. Time is measured in seconds along the X-‐axis, and latency is measured in seconds
along the Y-‐axis.
Part 4: Extrasystolic Contractions
Extrasystolic contractions were initiated and measured during late diastole. A
minimum voltage of 4.0V was determined to be the minimum voltage to provide an
extrasystolic contraction and was used as the threshold voltage, with an initial baseline
tension of 0.0-‐0.1g. After the extrasystolic contraction, a rest period of 10 beats was
provided before repeating the process. This was done for 3 trials (Table 1).
0.26
0.28
0.30
0.32
0.34
0 15 30 45 60 75 90 105 120
Latency (seconds)
Time (seconds)
Latency Between Mechanical and Electrical Activity
Latency (seconds)
7
Table 1: Contractile force of ventricular contraction in grams (g) before an extrasystole, for the extrasystole,
and immediately post extrasystole when a 4.0V stimulus was directly applied to the frog heart in late diastole.
Compensatory pause was measured in seconds (sec). Data for 3 trials as well as averages are shown.
Baseline tension was 0.0-‐0.1g.
Threshold voltage of 4.0V was doubled to 8.0V and the experiment was repeated.
Initial baseline tension was 0.0-‐0.1g and the stimulus was applied in late diastole. After the
extrasystolic contraction a rest period of 10 beats was provided to the frog heart before
repeating. Three trials were done and averages were taken and compensatory pause was
measured (Table 2).
Table 2: Contractile force of ventricular contraction measured in grams (g) before an extrasystole, for the
extrasystole, and immediately post extrasystole when an 8.0V stimulus was directly applied to the frog heart
in late diastole. Compensatory pause was measured in seconds (sec). Baseline tension was 0.0-‐0.1g.
An extrasystolic contraction was initiated in early diastole stimulating the frog heart
with a minimum threshold voltage measured at 5.0V. Initial baseline tension was 0.0-‐0.1g.
8
This was done one time. Measurements that were taken for the trial and compensatory
pause of the 5.0V direct stimulation of the frog heart in early diastole (Table 3).
Table 3: Contractile force of ventricular contraction in grams (g) before an extrasystole, for the extrasystole,
immediately post extrasystole when a 5.0V stimulus was directly applied to the frog heart in early diastole.
Compensatory pause was measured in seconds (sec). Baseline tension was 0.0-‐0.1g.
Part 5: Vagal Stimulation
An electrode was hooked onto the Vagus nerve of the frog with a piece of parafilm
isolating the electrode from tissue contact. The minimum threshold voltage to elicit
bradycardia was determined to be 2.75V by observing a decrease in contractile strength.
Contractile strength began at 1.19g and was observed over a 10 second time period with a
frequency of 20 pulses per second (pps) (Figure 5).
Figure 5: Ventricular contraction force measured before and after stimulating the Vagus nerve in the frog.
Stimulation was applied using an electrode directly attached to the nerve. Stimulation measured 2.75V at a
frequency of 20pps (pulse per second). Contractile force before stimulation measured 1.19g and after
stimulation measured 0.75g, declining after stimulation. Ventricular contraction force is measured in grams
along the X-‐axis. Baseline tension was 0.0-‐0.1g.
0 0.2 0.4 0.6 0.8 1 1.2 1.4
Contractile Force Before (g) Contractile Force After (g)
Ventricular Contraction Force (g)
Ventricular Contraction Force Before and After Vagal Stimulation During Bradycardia
9
Heart rate was monitored during the same 10-‐second time period and did not
change (Figure 6).
Figure 6: Heart Rate of 44.11 BPM (beats per minute) before and after stimulating the Vagus nerve in the
frog. Stimulation was applied using an electrode directly attached to the nerve. Stimulation measured 2.75V
at a frequency of 20pps (pulse per second). Beats per minute (BPM) are measured along the X-‐axis, and
remained unchanged.
Stimulus voltage was increased on the Vagus nerve to 4.0V to elicit cardiac arrest.
Initial heart rate was recorded for 30 seconds prior to stimulation and measured using the
5 beats prior to stimulation and averaged. Stimulation of the Vagus nerve was initiated at a
frequency of 20pps (pulse per second). Cardiac arrest lasted for 65 seconds before a
mechanical signal was next detected. A regular rhythm occurred at 81 seconds post
stimulation and Vagal stimulation was terminated. Post stimulation heart rate and
contraction tension were recorded using the 5 beats post termination and averaged (Table
4).
40 41 42 43 44 45
HR Before (BPM) HR After (BPM)
Beats Per Minute (BPM)
Heart Rate Before and After Vagal Stimulation During Bradycardia
10
Table 4: Measurements for initial activity prior to vagal stimulation and averaged. Baseline tension was 0.0-‐
0.1g. Average contractile tension was 1.01g and average heart rate was 42.98 BPM. Post Vagal stimulation
average contractile tension was 0.42g and average BPM was 31.27, decreasing in both categories, for the 5
beats immediately after Vagal stimulation of 4.0V at 20pps was terminated.
Comparing the initial heart rate with the post cardiac arrest heart rate identifies a
large decrease in BPM post cardiac arrest (Figure 7).
Figure 7: Initial heart rate measured 42.98 BPM. Post cardiac arrest heart rate was averaged at 31.27 BPM
for the 5 beats after stimulation of the Vagus nerve was terminated. Beats per minute (BPM) are measured
along the X-‐axis.
Comparing the initial ventricular contractile force with the post cardiac arrest
ventricular contractile force indicates a large drop in tension after cardiac arrest (Figure 8).
0 5 10 15 20 25 30 35 40 45 50
HR Before (BPM) HR After (BPM)
Beats Per Minute (BPM)
Heart Rate Before and After Cardiac Arrest
11
Figure 8: Initial ventricular contractile force measured 1.01g. Baseline tension was 0.0-‐0.1g. Post cardiac
arrest contractile force measured 0.42g for the 5 beats after stimulation of the Vagus nerve was terminated.
Tension is measured in grams along the X-‐axis.
Part 6: The Effects of Epinephrine
Epinephrine was injected in the frog’s heart 3 times. An initial tension (g) and heart
rate (BPM) were measured averaging the 5 beats immediately before the injections. BPM
was calculated from the beginning of phase 0 of the electrical signal to the same point of the
next signal. The 5 beats post injection and at 30 second intervals for 3 minutes were
averaged identically to the baseline measurements (Table 5).
Table 5: Initial average tension (g) of 0.48g and beats per minute (BPM) of 43.17 BPM compared with
measurements taken at 30-‐second intervals over a 3 minute time period. Baseline tension was 0.0-‐0.1g.
Averages were measured from the 5 beats immediately after each time point. Tension (g) increased 50% and
heart rate (BPM) increased 35.46% over baseline averages.
Average heart rate continued to increase over the 3 minute time period with the
largest % increase of 10.08% seen from 30 to 60 seconds (Figure 9).
0 0.2 0.4 0.6 0.8 1 1.2
Contractile Force Before (g) Contractile Force After (g)
Tension (g)
Ventricular Contraction Force Before and After Cardiac Arrest
12
Figure 9: Average heart rate (BPM) measured every 30 seconds for a 3-‐minute time period after injecting the
frog heart with epinephrine. Baseline tension was 0.0-‐0.1g. Initial heart rate measured 43.17 BPM and
continued to increase throughout the experiment. Ending average heart rate of 58.48 BPM was an increase of
35.46% over baseline. Averages were calculated with the 5 beats immediately after each time interval. Time
interval is measured in seconds along the X-‐axis and heart rate is measured in BPM along the Y-‐axis.
Average ventricular contraction force (g) peaked at 30 seconds with an 87.50%
increase over baseline tension (Figure 10).
Figure 10: Average ventricular contraction force (g) measured every 30 seconds for a 3-‐minute time period
after injecting the frog heart with epinephrine. Averages were measured from the 5 beats immediately after
each time point. Baseline tension was 0.0-‐0.1g. Tension initially increased and then decreased, ending with
an overall increase in contraction force. Initial tension measured 0.48g increasing 50% over the time period
to 0.72g. Peak tension was measured at 30 seconds of 0.92g, an 87.50% increase over initial tension. Time
interval is measured in seconds along the X-‐axis and ventricular contraction force is measured in grams along
the Y-‐axis.
30.00
40.00
50.00
60.00
Before 0 30 60 90 120 150 180
Heart Rate (BPM
)
Time Interval (seconds)
Average Heart Rate (BPM) at Varying Time Intervals
Heart Rate (BPM)
0.00
0.50
1.00
Before 0 30 60 90 120 150 180
Tension (g)
Time Interval (seconds)
Average Ventricular Contraction Force (g) at Varying Time Intervals
Tension (g)
13
Discussion:
Part 3: Electrical & Mechanical Activity of The Heart
Action potentials generated from autorhythmic cells in the sinus venosus of the frog
heart are spread to contractile cells to initiate contraction. The signals are transmitted
from cell to cell from a specialized structure called an intercalated disc. The intercalated
disc has two types of membrane junctions, desmosomes and gap junctions. Contraction in
the heart creates mechanical stress. Desmosomes provide the mechanical stability needed
to withstand this stress. Gap junctions are responsible for transmitting the electrical signal
from cell to cell (Sherwood, 2010, p. 308).
Atrial cells are separated from ventricular cells and contract separately and with
different amounts of force (Sherwood, 2010, p. 308). This can be observed from measuring
contraction tension and measuring the electrical activity of the cardiac cycle.
The atria generate less electrical activity than the ventricle does due to its smaller
size. When the atria contracts blood rushes to the ventricle, filling the ventricle. When the
ventricle fills and its pressure exceeds aortic pressure the aortic valve opens and blood
leaves the ventricle. This amount of blood leaving the ventricle is the stroke volume
(Sherwood, 2010, p. 323). This variance in mechanical activity was observed in the
measured atrial contraction force of 0.38g and the ventricular contraction force of 1.35g.
The Frank-‐Starling Law of The Heart explains the relationship between stroke
volume and ventricular contraction. The more stretched the ventricle becomes, that is the
larger the end diastolic volume, the larger the force of contraction will be, increasing stroke
volume (Widmaier, Raff, & Strang, 2004, p. 396).
14
Cardiac output is the amount of blood the ventricle pumps out per minute. This is
measured by evaluating the stroke volume and heart rate. Heart rate is regulated from the
electrical activity of the autorhythmic cells and is a result of ionic movement (Sherwood,
2010, p. 325).
Once a contractile cell receives a signal from an autorhythmic cell it begins its action
potential by opening fast Na+ channels and rapidly depolarizes. K+ transient channels
release K+ as the Na+ channels close providing an initial rapid repolarization period. Then
L-‐type Ca2+ channels slowly open creating a plateau phase, and voltage-‐gated K+ channels
rapidly flush out K+ bringing the membrane potential of the contractile cell back to
threshold (Sherwood, 2010, p. 314).
This cycle was used to measure heart rate in beats per minute on the frog heart.
The initial opening of the fast Na+ channels was identified as phase 0 and was measured to
the initiation of the next contraction cycle. The frog had an initial heart rate of 38.95 BPM.
There is a delay between the onset of a contraction from an action potential and the
actual response. This is known as the refractory period, and is to prevent tetanus in the
heart (Sherwood, 2010, p. 316). In the frog, latency between electrical activity and
contractile response was measured at 0.30 seconds. In a study on mammalian hearts of
rabbits, cats, and dogs it was found that this latency period, the absolute refractory period,
remains constant regardless of the heart rate (Dale & Drury, 1932, p. 222).
Sources of error in this experiment were due to an excess of adipose tissue in the
frog heart, inconsistent supply of Ringers solution, and outside movement of the subject’s
table.
Part 4: Extrasystolic Contractions
15
An extrasystolic contraction is also known as a premature ventricular contraction
(PVC) (Sherwood, 2010, p. 319). These occur during the relative refractory period in the
ventricular contractile cell and initiate a contraction before the cell has returned to it’s
resting membrane potential. Due to the extrasystolic contraction, there is an extra delay
before the next contraction occurs. This is known as compensatory pause, and is regulated
by the pacemaker activity in the heart.
A case study on a 68-‐year-‐old patient shows the mechanism of compensatory pause.
After analyzing recorded data from the patient, two beats occurring close together were
followed by a long pause (Carbone, Oreto, & Oreto, 2013, p. 90). This was seen in our
experiments on late diastole stimulation and early diastole stimulation.
It is expected that the extrasystolic contraction would have a greater force of
contraction due to the cell not fully returning to resting potential. In the experiments
conducted this was not seen. Minimum threshold voltage to elicit an extrasystolic
contraction during late diastole was found to be 4.0V. At this voltage the extrasystolic
contraction was found to be 0.03g less forceful than the initial contraction with a
compensatory pause of 0.94 seconds. When the voltage was doubled to 8.0V the
extrasystolic contraction results were the same, with a compensatory pause of 1.01
seconds. During the attempt on early diastole at 5.0V the extrasystolic contraction was
0.22g smaller than the initial contraction with a compensatory pause of 1.26 seconds.
Due to our inability to accurately and precisely initiate the stimulus in the relative
refractory period it was expected to not obtain predicted results. Additionally the frog
heart began to tear, Ringers solution was inconsistently applied, and there was outside
interference of the subject’s table.
16
Part 5: Vagal Stimulation
The Vagus nerve is the parasympathetic input to the heart. Parasympathetic
stimulation in the heart increases membrane permeability to K+ thus making it more
negative, or hyperpolarizing it, leading to a decrease in heart rate (Widmaier, Raff, &
Strang, 2004, p. 395). The Vagus nerve releases acetylcholine, which then binds to a
muscarinic receptor. A G-‐protein cascade occurs with this, inhibiting the cAMP pathway
activity. This ultimately inhibits phosphorylation and reduces activity of voltage-‐gated
channels required for contraction, leading to a decrease in heart rate and contractile force
(Sherwood, 2010, p. 326). This decrease in heart rate and contractile force was observed in
the experiment when cardiac arrest occurred, as expected. The presence of acetylcholine
made the heart unable to return to its pre-‐stimulation heart rate of 42.98 BPM and
contractile force of 1.01g, but would be expected to return to normal heart rate and force of
contraction with time. This was shown in an experiment on mongrel dogs, and gradually
the heart rate did return to normal (Campos & Friedman, 1963, p. 251).
During bradycardia the heart rate slows (Sherwood, 2010, p. 319). The same
experiment on mongrel dogs shows this effect, however was not seen in our experiment on
the frog heart(Campos & Friedman, 1963, p. 251). There was a reduction in contractile
force from 1.19g to 0.75g, however heart rate remained unchanged. This could be due to
not enough stimulus voltage to elicit a delay in rate of beating, or not stimulating the Vagus
nerve for enough time to allow acetylcholine to appropriately inhibit it’s factors.
Additionally in the experiment there was excess Ringers solution, which may have altered
the electrical stimulation on the nerve.
Part 6: The Effects of Epinephrine
17
Opposite of the Vagus nerve, epinephrine is the resultant effect of stimulation of the
sympathetic nervous system. The experiment involved injecting the frog heart with
epinephrine, was administered 3 times, and deviated from the lab manual.
The sympathetic nervous system impacts heart rate and contractile force in times of
need for an increase of such factors, such as in times of exercise or emergency (Sherwood,
2010, p. 327). Antagonistic to acetylcholine, epinephrine increases rate of depolarization
in the cardiac cells leading to an increase in rate of contraction. This increase in rate of
contraction leads to an increase in heart rate and contractile force ultimately increasing
stroke volume and cardiac output (Sherwood, 2010, p. 328).
Epinephrine acts on beta-‐adrenergic receptors in the main pacemaker of the heart.
These receptors stimulate a G-‐protein cascade increasing the cAMP pathway activity in
cardiac cells, increasing phosphorylation. This allows energy requiring processes, such as
the voltage-‐gated channels used in contraction, to remain open longer. This will ultimately
increase contractile strength, and additionally decrease delay between beats of the heart
(Sherwood, 2010, p. 327).
This mechanism was seen in the experiments on the frog heart with an increase in
heart rate of 35.46% over the 3-‐minute data sample. An experiment on bull calves showed
similar results to heart rate increase when injected with epinephrine (Stewart & Webster,
2010, p. 5252).
Contractility has a greater effect with increased presence of epinephrine due to the
greater influx of Ca2+ into the contractile cell. From this increased concentration of
intracellular Ca2+ there is greater cross-‐bridge cycling and the myocardial fibers are able to
generate more force. This process ultimately increases stroke volume leading to an
18
increase in cardiac output, ultimately shifting the Frank-‐Starling curve inward (Sherwood,
2010, p. 329).
This increase in contractility was seen in our experiment with an overall increase of
50% over the 3-‐minute time period. However, due to tearing of the heart muscle and
inconsistent application of Ringers solution the contractile force declined after the 30-‐
second measurement.
19
References: Bautista, E., & Korber, J. (2009). NPB 101L Physiology Lab Manual (2nd Edition). Mason,
Ohio: Cengage Learning, 43-‐54. Campos, H., & Friedman, A. (1963). The Influence of Acute Sympathetic Denervation,
Reserpine and Choline Xylyl Ether on Vagal Escape. Journal of Physiology , 169, 249-‐262.
Carbone, V., Oreto, L., & Oreto, G. (2013). Ventricular Extrasystoles with Interpolation or
Postponed Compensatory Pause during Atrial Fibrillation: Fact or Fiction? Annals of Noninvasive Electrocardiology , 18 (1), 90-‐94.
Dale, A., & Drury, A. (1932). The refractory period of mamalian cardiac muscle, with
especial reference to purkinje tissue. The Journal of Physiology, 76 (2), 201-‐223. Faller, A. (2004). The Human Body: An Introduction to Structure and Function (13th
Edition). Stuttgart, Germany: Thieme, 214. Sherwood, L. (2010). Human Physiology: From Cells to Systems (7th Edition). Belmont:
Brooks/Cole, 308-‐329. Stewart, M., & Webster, J. (2010). Technical note: Effects of an epinephrine infusion on eye
temperature and heart rate variability in bull calves. Journal of Dairy Science, 93 (11), 5252-‐5257.
Widmaier, E., Raff, H., & Strang, K. (2004). Vander, Sherman, & Luciano's Human Physiology:
The Mechanisms of Body Function (9th Edition). New York: McGraw Hill, 394-‐396.
Raw Data:
20
Average Atrial Contraction Force
Average Ventricle Contraction Force
Average Heart Rate
21
Latency between electrical and mechanical activity
Extrasystole obtained from 4.0V stimulation during late diastole
22
Extrasystole obtained from 8.0V stimulation during late diastole
Extrasystole obtained from 5.0V stimulation during early diastole
23
Vagal nerve stimulation at 2.75V for 10 seconds to elicit bradycardia
Cardiac Arrest/Vagal Escape at 4.0V
24
Effects of Epinephrine – Before Injection
Effects of Epinephrine – Immediately Post Injection
25
Effects of Epinephrine – 30 seconds Post Injection
Effects of Epinephrine – 60 Seconds Post Injection
26
Effects of Epinephrine – 90 Seconds Post Injection
Effects of Epinephrine – 120 Seconds Post Injection
27
Effects of Epinephrine – 150 Seconds Post Injection
Effects of Epinephrine – 180 Seconds Post Injection
28