Sarcolemmal KATP channel triggers delayed ischemic preconditioning in rats

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Title Sarcolemmal KATP channel triggers delayed ischemic preconditioning in rats
Author Patel, Hemal H.; Gross, Eric R.; Peart, Jason Nigel John; Hsu, Anna K.; Gross, Garrett J.
Journal Name American Journal of Physiology: Heart and Circulatory Physiology
Year Published 2005
Place of publication United States
Publisher American Physiological Society
Abstract 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 -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 sKATP or mKATP. 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 sKATP channel antagonist, HMR-1098 (6 mg/kg), or the selective mKATP 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 sKATP channel is required as a trigger but not a mediator for delayed IPC-induced infarct size reduction in rat hearts.
Peer Reviewed Yes
Published Yes
Alternative URI http://dx.doi.org/10.1152/ajpheart.00031.2004
Volume 288
Issue Number 1
Page from H445
Page to H447
ISSN 0363-6135
Date Accessioned 2006-07-26
Date Available 2009-09-28T06:51:22Z
Language en_AU
Research Centre Griffith Health Institute; Heart Foundation Research Centre
Faculty Griffith Health Faculty
Subject PRE2009-Clinical Pharmacology and Therapeutics
URI http://hdl.handle.net/10072/25831
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1x

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