alexa Sex-specific and exercise-acquired cardioprotection is abolished by sarcolemmal KATP channel blockade in the rat heart.
Cardiology

Cardiology

Journal of Clinical & Experimental Cardiology

Author(s): Chicco AJ, Johnson MS, Armstrong CJ, Lynch JM, Gardner RT,

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Abstract The present study was conducted to determine whether the infarct sparing effect of short-term exercise is dependent on the operation of the myocardial sarcolemmal ATP-sensitive K(+) (K(ATP)) channel. Adult male and female Sprague-Dawley rats were exercised on a motorized treadmill for 5 days. Twenty-four hours following the training or sedentary period, hearts were isolated and exposed to 1 h of regional ischemia followed by 2 h of reperfusion on a modified Langendorf apparatus in the presence or absence of the sarcolemmal K(ATP) channel antagonist HMR-1098 (30 microM). Following the ischemia-reperfusion protocol, infarct size was determined as a percentage of the total ischemic zone at risk (ZAR). Short-term exercise reduced infarct size by 24\% in males (32 +/- 2\% of ZAR; P < 0.01) and by 18\% in females (26 +/- 2\% of ZAR; P < 0.05). Sarcolemmal K(ATP) channel blockade abolished the training-induced cardioprotection in both males and females, increasing infarct size to 43 +/- 3\% and 52 +/- 4\% of ZAR, respectively. In the absence of HMR-1098, infarct size was significantly lower in sedentary females than in males (33 +/- 4\% vs. 42 +/- 2\% of ZAR, respectively; P < 0.01). However, the presence of HMR-1098 abolished this sex difference, increasing infarct size by 58\% in the sedentary females (P < 0.01) but having no effect on infarct size in sedentary males. This study demonstrates that the sex-specific and exercise-acquired resistance to myocardial ischemia-reperfusion injury is dependent on sarcolemmal K(ATP) activity during ischemia. This article was published in Am J Physiol Heart Circ Physiol and referenced in Journal of Clinical & Experimental Cardiology

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