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1 Cardiovascular Research Institute, University of California, San Francisco, California 94143; and 2 Outcomes Research Institute and Department of Anesthesiology, University of Louisville, Louisville, Kentucky 40202
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 with 99mTc-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.
hypothermia; ischemia-reperfusion injury; myocardial infarction; myocyte viability
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