Show simple item record

dc.contributor.authorHeadrick, Johnen_US
dc.contributor.authorGauthier, NS.en_US
dc.contributor.authorMatherne, GP.en_US
dc.date.accessioned2017-05-03T13:44:13Z
dc.date.available2017-05-03T13:44:13Z
dc.date.issued2000en_US
dc.identifier.issn03636135en_US
dc.identifier.urihttp://hdl.handle.net/10072/3466
dc.description.abstractWe studied the role of mitochondrial ATP-sensitive K+(KATP) channels in modifying functional responses to 20 min global ischemia and 30 min reperfusion in wild-type mouse hearts and in hearts with ~250-fold overexpression of functionally coupled A1-adenosine receptors (A1ARs). In wild-type hearts, time to onset of contracture (TOC) was 303 ᠲ4 s, with a peak contracture of 89 ᠵ mmHg. Diastolic pressure remained elevated at 52 ᠶ mmHg after reperfusion, and developed pressure recovered to 40 ᠶ% of preischemia. A1AR overexpression markedly prolonged TOC to 517 ᠸ4 s, reduced contracture to 64 ᠶ mmHg, and improved recovery of diastolic (to 9 ᠴ mmHg) and developed pressure (to 82 ᠸ%). 5-Hydroxydecanoate (5-HD; 100 卩, a mitochondrial KATPblocker, did not alter ischemic contracture in wild-type hearts, but increased diastolic pressure to 69 ᠸ mmHg and reduced developed pressure to 10 ᠵ% during reperfusion. In transgenic hearts, 5-HD reduced TOC to 348 ᠱ8 s, increased postischemic contracture to 53 ᠴ mmHg, and reduced recovery of developed pressure to 22 ᠴ%. In summary, these data are the first to demonstrate that endogenous activation of KATP channels improves tolerance to ischemia-reperfusion in murine myocardium. This functional protection occurs without modification of ischemic contracture. The data also support a role for mitochondrial KATP channel activation in the pronounced cardioprotection afforded by overexpression of myocardial A1ARs.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherAmerican Physiological Societyen_US
dc.publisher.placeUSAen_US
dc.publisher.urihttp://ajpheart.physiology.org/content/279/4/H1690en_US
dc.relation.ispartofpagefromH1690en_US
dc.relation.ispartofpagetoH1697en_US
dc.relation.ispartofjournalAmerican Journal of Physiology: Heart and Circulatory Physiologyen_US
dc.relation.ispartofvolume279en_US
dc.subject.fieldofresearchcode320000en_US
dc.titleCardioprotection by KATP channels in wild-type hearts and hearts overexpressing A1 adenosine receptorsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_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.issued2015-02-05T03:42:49Z
gro.hasfulltextNo Full Text


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record