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Am J Physiol Heart Circ Physiol 283: H1538-H1544, 2002. First published June 27, 2002; doi:10.1152/ajpheart.00040.2002
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Vol. 283, Issue 4, H1538-H1544, October 2002

Cardioprotection by multiple preconditioning cycles does not require mitochondrial KATP channels in pigs

Lisa M. Schwartz, Timothy S. Welch, and Mark S. Crago

Department of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799

To test whether cardioprotection induced by ischemic preconditioning depends on the opening of mitochondrial ATP-sensitive K+ (KATP) channels, the effect of channel blockade was studied in barbital-anesthetized open-chest pigs subjected to 30 min of complete occlusion of the left anterior descending coronary artery and 3 h of reflow. Preconditioning was elicited by two cycles of 5-min occlusion plus 10-min reperfusion before the 30-min occlusion period. 5-Hydroxydecanoate (5 mg/kg iv) was injected 15 min before preconditioning or pharmacological preconditioning induced by diazoxide (3.5 mg/kg, 1 ml/min iv). Infarct size (percentage of the area at risk) after 30 min of ischemia was 35.1 ± 9.9% (n = 7). Preconditioning markedly limited myocardial infarct size (2.7 ± 1.6%, n = 7), and 5-hydroxydecanoate did not abolish protection (2.4 ± 0.9%, n = 8). Diazoxide infusion also significantly limited infarct size (14.6 ± 7.4%, n = 7), and 5-hydroxydecanoate blocked this effect (30.8 ± 8.0%, n = 7). Thus the opening of mitochondrial KATP channels is cardioprotective in pigs, but these data do not support the hypothesis that opening of mitochondrial KATP channels is required for the endogenous protection afforded by preconditioning.

heart; infarction; ischemia; 5-hydroxydecanoate; diazoxide; mitochondria; ischemic preconditioning


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