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Am J Physiol Heart Circ Physiol (November 24, 2004). doi:10.1152/ajpheart.00031.2004
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Submitted on January 13, 2004
Accepted on August 30, 2004

The Sarcolemmal KATP Channel Triggers Delayed Ischemic Preconditioning in Rats

Hemal H Patel1, Eric R Gross1, Jason N Peart1, Anna K Hsu1, and Garrett J Gross1*

1 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: ggross{at}mcw.edu.

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




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