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Postconditioning Does Not Reduce Myocardial Infarct Size in an In Vivo Regional Ischemia Rodent Model

The Heart Institute, Good Samaritan Hospital (JD, RAK), and Division of Cardiovascular Medicine (RAK), Keck School of Medicine, University of Southern California, Los Angeles, California

Robert A. Kloner, MD, PhD

The Heart Institute, Good Samaritan Hospital (JD, RAK), and Division of Cardiovascular Medicine (RAK), Keck School of Medicine, University of Southern California, Los Angeles, California, rkloner{at}goodsam.org

In our laboratory, postconditioning reliably reduces lethal ventricular arrhythmias in an in vivo rat model but its effect on necrosis in our model is unknown. In the present analysis, we tested a variety of postconditioning regimens in anesthetized rats subjected to 45 minutes of coronary occlusion and 120 minutes of reperfusion or 30 minutes of coronary occlusion and 120 minutes of reperfusion. In all studies, area at risk was determined by the blue dye technique and area of necrosis was assessed with triphenyl tetrazolium chloride staining and computerized planimetry of ventricular slices. Postconditioning regimens included 4 cycles of 10 seconds of reperfusion/10 seconds of reocclusion, 4 cycles of 20 seconds of reperfusion/20 seconds of reocclusion, 8 cycles of 30 seconds of reperfusion/30 seconds of reocclusion, and 20 cycles of 10 seconds of reperfusion/10 seconds of reocclusion. Postconditioning did not reduce myocardial infarct size with any of these regimens.

Key Words: myocardial infarct size • myocardial infarction • ST elevation myocardial infarction • postconditioning • preconditioning • reperfusion • reperfusion injury.

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