Effect of endovascular cooling on myocardial temperature, infarct size, and cardiac output in human-sized pigs
| Autor: | Michael W. Dae, Dong Wei Gao, Daniel I. Sessler, Kamel Chair, Carol A. Stillson |
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| Rok vydání: | 2002 |
| Předmět: |
Male
Technetium Tc 99m Sestamibi medicine.medical_specialty Cardiac output Swine Physiology Myocardial Infarction Myocardial Ischemia Ischemia Hemodynamics Myocardial Reperfusion Body Temperature Heart Rate Hypothermia Induced Physiology (medical) Internal medicine medicine Animals Myocardial infarction Cardiac Output Radionuclide Imaging business.industry Myocardium Heart Stroke Volume Blood flow Thermoregulation Hypothermia medicine.disease Coronary Vessels Radiography Anesthesia Circulatory system Cardiology Autoradiography Body Constitution Female medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 282:H1584-H1591 |
| ISSN: | 1522-1539 0363-6135 |
| Popis: | Mild hypothermia reduces myocardial infarct size in small animals; however, the extent of myocardial protection in large animals with greater thermal mass remains unknown. We evaluated the effects of mild endovascular cooling on myocardial temperature, infarct size, and cardiac output in 60- to 80-kg isoflurane-anesthetized pigs. We occluded the left anterior descending coronary artery for 60 min, followed by reperfusion for 3 h. An endovascular heat-exchange catheter was used to either lower core body temperature to 34°C ( n = 11) or maintain temperature at 38°C ( n = 11). Additional studies assessed myocardial viability and microvascular perfusion with99mTc-sestamibi autoradiography. Endovascular cooling reduced infarct size compared with normothermia (9 ± 6% vs. 45 ± 8% of the area at risk; P < 0.001), whereas the area at risk was comparable (19 ± 3% vs. 20 ± 7%; P = 0.65). Salvaged myocardium showed normal sestamibi uptake, confirming intact microvascular flow and myocyte viability. Cardiac output was maintained in hypothermic hearts because of an increase in stroke volume, despite a decrease in heart rate. Mild endovascular cooling to 34°C lowers myocardial temperature sufficiently in human-sized hearts to cause a substantial cardioprotective effect, preserve microvascular flow, and maintain cardiac output. |
| Databáze: | OpenAIRE |
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