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Sarcolemmal K_ATP channel triggers delayed ischemic preconditioning in rats

Medical College of Wisconsin, Department of Pharmacology and Toxicology, Milwaukee, Wisconsin

Submitted 13 January 2004 ; accepted in final form 30 August 2004

Previous work from our laboratory has shown that the sarcolemmal K_ATP channel (sK_ATP) is required as a trigger for delayed cardioprotection upon exogenous opioid administration. We also established that the mitochondrial K_ATP (mK_ATP) channel is not required for triggering delayed -opioid-induced infarct size reduction. Because mechanistic differences have been found among -opioids and that due to ischemic preconditioning (IPC), we determined whether the triggering mechanism of delayed IPC-induced infarct size reduction involves either the sK_ATP or mK_ATP. Male Sprague-Dawley rats received either sham surgery or IPC (3- to 5-min cycles of ischemia and reperfusion) 24 h before being subjected to 30 min of ischemia and 2 h of reperfusion. Infarct size was determined and expressed as a percentage of the area at risk, with significance compared with sham reported at P 0.001. A subset of both sham and IPC-treated rats received either the selective sK_ATP channel antagonist, HMR-1098 (6 mg/kg), or the selective mK_ATP channel antagonist, 5-hydroxydeconoic acid (5-HD; 10 mg/kg), given 5 min before IPC. Rats subjected to IPC demonstrated a significant reduction in infarct size compared with sham (29.2 ± 4.7 vs. 59.3 ± 2.5%, respectively; P 0.001). Prior administration of HMR-1098, but not 5-HD, abolished IPC-induced infarct size reduction (48.8 ± 2.9 and 28.8 ± 4.0%, respectively; P 0.001). Furthermore, administration of HMR 24 h after IPC, before index ischemia, did not abrogate IPC-induced infarct size reduction (33.0 ± 5.0 vs. 29.2 ± 4.7%, respectively; P 0.001). These data suggest that the sK_ATP channel is required as a trigger but not a mediator for delayed IPC-induced infarct size reduction in rat hearts.

5-hydroxydeconoic acid; HMR-1098

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