Therapeutic hypothermia improves cardiac function after ...effect of therapeutic hypothermia for...
1
Myocardial infarction Therapeutic hypothermia improves cardiac function after successful resuscitation from cardiac arrest in a rat model of myocardial infarction H. Li 1,5 , J. Park 1 , Y. Weng 1 , W. Wang 1 , T. Hua 1 , X. Wu 1 , M. Peberdy 1,2 , J. Ornato 1,3 and W. Tang 1,3,4 1 Weil Institute of Emergency and Critical Care Research at VCU,VA 2 Department of Internal Medicine, VCU, VA 3 Department of Emergency Medicine, VCU, VA 4 Sun Yat-sen Memorial Hospital, SunYat-sen University, Guangzhou, P.R China, 5 Department of Critical Care Medicine, The First Affiliated Hospital, Xi’an Jiaotong University , Xi’an, P.R China Results Background Methods Our previous studies have demonstrated that hypothermia therapy improves post-resuscitation cardiac function in cardiac arrest animal models. However, the animals which are involved in our models are healthy rats or swine . Since the majority of the cardiac arrest patients have coronary artery diseases, we investigated the effects of therapeutic hypothermia in a rat model of cardiac arrest with myocardial infarction. We hypothesized that therapeutic hypothermia provides a myocardial protective effect following resuscitation in animals with acute myocardial infarction. Animal Model Animals were anesthetized and intubated, followed by left anterior descending coronary artery (LAD) ligation for establishment of acute myocardial infarction. The chest was closed after ligation. Catheters were then inserted at the femoral vein, femoral artery, and external jugular vein. A guidewire was advanced into the right ventricle to induce ventricular fibrillation (VF) via electrical stimulation. Precordial compression and ventilation were started after onset of untreated VF. Resuscitation was attempted with up to three 2-J counter shocks after CPR. 1. Kelly FE, Nolan Jp. The effects of mild induced hypothermia on the myocardium: a systematic review. Anaesthesia 2010; 65:505-15. 2.Hus CY, Huang CH, Chang WT, et al. Cardioprotective effect of therapeutic hypothermia for postresuscitation myocardial dysfunction. Shock 2009; 32:210-6. Table1. There was no difference in body weight, mean arterial pressure, and end-tidal C02 between two groups at baseline and PR 4hrs Conclusions Therapeutic hypothermia reduces the severity of post-resuscitation myocardial dysfunction in a rat model of acute myocardial infarction. Figure 1. There was no difference in lactate (A) and blood glucose (B) between the two groups at baseline, PR 1hr, and PR 4hrs. Figure 3. There was an improvement in left ventricular ejection fraction (A) and cardiac output (B) in MI-HT animals treated with hypothermia therapy beginning at PR 30 min when compared with MI-NT animals. Figure 4. Left parasternal long axis Doppler echocardiogram of the left ventricle outflow tract and aorta showed the blood flow rate in MI-HT group (A) was higher than MI-NT group (B) Figure 2. The blood temperature of the MI-HT group was decreased at 32°C at PR 30min, and maintained for 4hrs (A) . The heart rate of MI- HT was lower with decreased temperature (B). MI-NT (N=6) MI-HT (N=6) P Body weight, g 516.33±12.34 518.33±22.19 0.898 Mean arterial pressure, mmHg Baseline 141.67±10.41 143.33±3.79 0.807 PR 4 hrs 88.43±17.27 115.70±7.09 0.072 End-tidal CO2, mmHg Baseline 41.67±1.15 40.00±1.15 0.323 PR 4 hrs 30.47±4.01 38.33±1.53 0.069 A B A A B B A B References Animals were randomized into 2 groups: (1) Acute myocardial infarction-Normothermia group (MI-NT group, n=6): the rats underwent LAD ligation 90 min before the induction of VF, after restoration of spontaneous circulation (ROSC), the core temperature was maintained at 37.0±0.2°C by a heating blanket; (2) Acute myocardial infarction-Hyopthermia group (MI-HT group, n=6): the treatment was identical to the AMI-NT group, and after ROSC the temperature was maintained at 32.0±0.5°C by a cooling blanket. The post- resuscitation cardiac function was evaluated by echocardiography in all animals. Experimental Protocol 2 μ m 2 μ m K O K O m LAD ligation VF PC Post Resuscitation Normothermia or Hypothermia Insert catheters Defibrillation Echocardiography Methods Femoral artery catheter Temperature monitor Guidewire for induction VF External jugular vein catheter Electrical stimulation box Femoral vein catheter ST wave elevation Tracheal intubation Electrocardiogram Blood pressure Right atrium pressure End tidal CO2 LAD ligation Biopsy and Electrocardiogram Normal Myocardial infarction -90 min Baseline 0 6min 14min 30min 60min 120min 180min 240min Infarction area LAD ligation Disclosure None
Transcript of Therapeutic hypothermia improves cardiac function after ...effect of therapeutic hypothermia for...
Myocardial infarction
Therapeutic hypothermia improves cardiac function after successful
resuscitation from cardiac arrest in a rat model of myocardial infarctionH. Li1,5, J. Park1, Y. Weng1, W. Wang1, T. Hua1, X. Wu1, M. Peberdy1,2, J. Ornato1,3 and W. Tang1,3,4
1Weil Institute of Emergency and Critical Care Research at VCU,VA 2Department of Internal Medicine, VCU, VA 3Department of Emergency
Medicine, VCU, VA 4 Sun Yat-sen Memorial Hospital, SunYat-sen University, Guangzhou, P.R China, 5Department of Critical Care Medicine,
The First Affiliated Hospital, Xi’an Jiaotong University , Xi’an, P.R China
ResultsBackground
Methods
Our previous studies have demonstrated that hypothermia
therapy improves post-resuscitation cardiac function in
cardiac arrest animal models. However, the animals which
are involved in our models are healthy rats or swine . Since
the majority of the cardiac arrest patients have coronary
artery diseases, we investigated the effects of therapeutic
hypothermia in a rat model of cardiac arrest with
myocardial infarction. We hypothesized that therapeutic
hypothermia provides a myocardial protective effect
following resuscitation in animals with acute myocardial
infarction.
Animal Model
Animals were anesthetized and intubated, followed by
left anterior descending coronary artery (LAD) ligation for
establishment of acute myocardial infarction. The chest
was closed after ligation. Catheters were then inserted at
the femoral vein, femoral artery, and external jugular
vein. A guidewire was advanced into the right ventricle
to induce ventricular fibrillation (VF) via electrical
stimulation. Precordial compression and ventilation
were started after onset of untreated VF. Resuscitation
was attempted with up to three 2-J counter shocks after
CPR.
1. Kelly FE, Nolan Jp. The effects of mild induced
hypothermia on the myocardium: a systematic review.
Anaesthesia 2010; 65:505-15.
2. Hus CY, Huang CH, Chang WT, et al. Cardioprotective
effect of therapeutic hypothermia for postresuscitation
myocardial dysfunction. Shock 2009; 32:210-6.
Table1. There was no difference in body weight, mean arterial pressure, and end-tidal C02 between two groups at baseline and PR 4hrs
Conclusions
Therapeutic hypothermia reduces the severity
of post-resuscitation myocardial dysfunction in
a rat model of acute myocardial infarction.
Figure 1. There was no difference in lactate (A) and blood glucose (B) between the two groups at baseline, PR 1hr, and PR 4hrs.
Figure 3. There was an improvement in left ventricular ejectionfraction (A) and cardiac output (B) in MI-HT animals treated withhypothermia therapy beginning at PR 30 min when compared withMI-NT animals.
Figure 4. Left parasternal long axis Doppler echocardiogram of theleft ventricle outflow tract and aorta showed the blood flow rate inMI-HT group (A) was higher than MI-NT group (B)
Figure 2. The blood temperature of the MI-HT group was decreased at 32°C at PR 30min, and maintained for 4hrs (A) . The heart rate of MI-HT was lower with decreased temperature (B).
MI-NT (N=6) MI-HT (N=6) P
Body weight, g 516.33±12.34 518.33±22.19 0.898
Mean arterial pressure, mmHg
Baseline 141.67±10.41 143.33±3.79 0.807
PR 4 hrs 88.43±17.27 115.70±7.09 0.072
End-tidal CO2, mmHg
Baseline 41.67±1.15 40.00±1.15 0.323
PR 4 hrs 30.47±4.01 38.33±1.53 0.069
A B A
A B
B
A B
References
Animals were randomized into 2 groups: (1) Acute
myocardial infarction-Normothermia group (MI-NT group,
n=6): the rats underwent LAD ligation 90 min before the
induction of VF, after restoration of spontaneous
circulation (ROSC), the core temperature was
maintained at 37.0±0.2°C by a heating blanket; (2)
Acute myocardial infarction-Hyopthermia group (MI-HT
group, n=6): the treatment was identical to the AMI-NT
group, and after ROSC the temperature was maintained
at 32.0±0.5°C by a cooling blanket. The post-
resuscitation cardiac function was evaluated by
echocardiography in all animals.
Experimental Protocol
2
μ
m
K
O
2
μ
m
K
O
K
O
2
μ
m
LAD ligation
VF PC Post Resuscitation
Normothermia or Hypothermia
Insert catheters
Defibrillation
Echocardiography
Methods
Femoral artery catheter
Temperature monitor
Guidewire for induction VF
External jugular vein
catheter
Electrical stimulation box
Femoral vein catheter
ST wave elevation
Tracheal intubation
Electrocardiogram
Blood pressure
Right atrium pressure
End tidal CO2
LAD ligation
Biopsy and Electrocardiogram
Normal Myocardial infarction
-90 min Baseline 0 6min 14min 30min 60min 120min 180min 240min
Infarction area
LAD ligation Disclosure
None
![Therapeutic Hypothermia in Traumatic Brain Injurycdn.intechopen.com/pdfs/42406/InTech-Therapeutic... · 80 Therapeutic Hypothermia in Brain Injury hypothermia [13-50]. In addition,](https://static.fdocuments.in/doc/165x107/5e902d36c9c187069d5dbc10/therapeutic-hypothermia-in-traumatic-brain-80-therapeutic-hypothermia-in-brain-injury.jpg)
