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dc.contributor.authorH. Patel, Hemalen_US
dc.contributor.authorR. Gross, Ericen_US
dc.contributor.authorN. Peart, Jasonen_US
dc.contributor.authorK. Hsu, Annaen_US
dc.contributor.authorJ. Gross, Garretten_US
dc.date.accessioned2017-04-24T10:09:13Z
dc.date.available2017-04-24T10:09:13Z
dc.date.issued2005en_US
dc.identifier.issn03636135en_US
dc.identifier.doi10.1152/ajpheart.00031.2004en_US
dc.identifier.urihttp://hdl.handle.net/10072/25831
dc.description.abstractPrevious 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 ᠴ.7 vs. 59.3 ᠲ.5%, respectively; P 0.001). Prior administration of HMR-1098, but not 5-HD, abolished IPC-induced infarct size reduction (48.8 ᠲ.9 and 28.8 ᠴ.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 ᠵ.0 vs. 29.2 ᠴ.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.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherAmerican Physiological Societyen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofpagefromH445en_US
dc.relation.ispartofpagetoH447en_US
dc.relation.ispartofissue1en_US
dc.relation.ispartofjournalAmerican Journal of Physiology: Heart and Circulatory Physiologyen_US
dc.relation.ispartofvolume288en_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchcode320503en_US
dc.titleSarcolemmal KATP channel triggers delayed ischemic preconditioning in ratsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
gro.date.issued2015-02-05T03:43:31Z
gro.hasfulltextNo Full Text


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