Sharon L Hale1, Robert A Kloner. 1. Heart Institute of Good Samaritan Hospital and Department of Medicine, University of Southern California, Los Angeles, California 90017, USA. sharon.hale@attglobal.net
Abstract
PURPOSE: The effects of an elevated body temperature on infarct size were tested in a rabbit model of ischemia/reperfusion. METHODS: Before coronary artery occlusion, body temperature was raised from baseline at 38.6 +/- 0.1 degrees C to 40.3 +/- 0.2 degrees C in nine treated rabbits. Temperature in eight normothermic rabbits was 38.4 +/- 0.2 degrees C. Both groups received 30 min coronary occlusion and 3 h reperfusion. RESULTS: In normothermic rabbits, 36 +/- 6% of the ischemic risk region became necrotic but in hyperthermic rabbits myocardial necrosis was significantly increased to 57 +/- 3% of the risk region (P < 0.005) despite similar risk regions and an equal degree of regional myocardial blood flow (RMBF) reduction during ischemia in both groups. Infarct size correlated positively with body temperature (r = 0.66, P < 0.004). RMBF was 43% lower during reperfusion in the previously ischemic areas of hyperthermic hearts compared with the control group (P < 0.04), suggesting worsened no-reflow. CONCLUSION: Elevation in body temperature by even a few degrees can aggravate necrosis during acute myocardial infarction and worsens no-reflow.
PURPOSE: The effects of an elevated body temperature on infarct size were tested in a rabbit model of ischemia/reperfusion. METHODS: Before coronary artery occlusion, body temperature was raised from baseline at 38.6 +/- 0.1 degrees C to 40.3 +/- 0.2 degrees C in nine treated rabbits. Temperature in eight normothermic rabbits was 38.4 +/- 0.2 degrees C. Both groups received 30 min coronary occlusion and 3 h reperfusion. RESULTS: In normothermic rabbits, 36 +/- 6% of the ischemic risk region became necrotic but in hyperthermic rabbits myocardial necrosis was significantly increased to 57 +/- 3% of the risk region (P < 0.005) despite similar risk regions and an equal degree of regional myocardial blood flow (RMBF) reduction during ischemia in both groups. Infarct size correlated positively with body temperature (r = 0.66, P < 0.004). RMBF was 43% lower during reperfusion in the previously ischemic areas of hyperthermic hearts compared with the control group (P < 0.04), suggesting worsened no-reflow. CONCLUSION: Elevation in body temperature by even a few degrees can aggravate necrosis during acute myocardial infarction and worsens no-reflow.
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