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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00040.2002
Submitted on January 20, 2002
Accepted on June 21, 2002
1 Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA
* To whom correspondence should be addressed. E-mail: lschwartz{at}usuhs.mil.
To test whether cardioprotection induced by ischemic preconditioning depends on opening mitochondrial KATP channels, the effect of channel blockade was studied in barbital-anesthetized open-chest pigs subjected to 30 min complete occlusion of the left anterior descending coronary artery and 3 h 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, i.v.) was injected 15 min before preconditioning, or pharmacological preconditioning induced by diazoxide (3.5 mg/kg, 1 ml/min, i.v.). Infarct size (percent of the area-at risk) following 30 min 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, opening mitochondrial KATP channels is cardioprotective in pigs, but these data do not support the hypothesis that opening mitochondrial KATP channels is required for the endogenous protection afforded by preconditioning.
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