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dc.contributor.authorZatta, Amandaen_US
dc.contributor.authorHack, Benjaminen_US
dc.contributor.authorHeadrick, Johnen_US
dc.date.accessioned2017-05-03T11:16:51Z
dc.date.available2017-05-03T11:16:51Z
dc.date.issued2003en_US
dc.date.modified2007-03-15T21:37:03Z
dc.identifier.issn03051870en_US
dc.identifier.doi10.1046/j.1440-1681.2003.03814.xen_AU
dc.identifier.urihttp://hdl.handle.net/10072/6133
dc.description.abstract1. Whether pyruvate inhibits or can actually initiate myocardial preconditioning is unclear and whether pyruvate provides protection via its action as a 'cosubstrate' with glucose or via alternative mechanisms also remains controversial. We examined effects of a high concentration of pyruvate (10 mmol/L) alone or with 15 mmol/L glucose in mouse hearts subjected to 20 min ischaemia and 30 min reperfusion. 2. Provision of 10 mmol/L pyruvate alone or as a cosubstrate markedly reduced ischaemic contracture and enhanced postischaemic recovery. Time to contracture was increased from approximately 3 min to over 8 min, peak contracture was reduced from 90 mmHg to less than 60 mmHg and postischaemic pressure development was also improved. Effects on contracture were independent of the presence of pyruvate during ischaemia and improved postischaemic recovery was evident with pre-ischaemic pyruvate perfusion. 3. Cardioprotection did not require the presence of pyruvate during ischaemia or reperfusion and effects of pyruvate pretreatment could be mimicked by pretreatment with 1 mmol/L dichloroacetate (DCA), an activator of pyruvate dehydrogenase. 4. Myocardial adenosine efflux and Ca2+ content were elevated (by 215 and 65%, respectively) following pretreatment with pyruvate, potentially triggering a preconditioned state. A role for adenosine A1 receptors is supported by lack of added protection with pyruvate in hearts transgenically overexpressing adenosine A1 receptors. 5. Collectively, these observations demonstrate that pre-ischaemic treatment with pyruvate or DCA provides a beneficial preconditioning-like effect in ischaemic and postischaemic myocardium. The response appears unrelated to glycolytic inhibition, but may be mediated via transient changes in adenosine levels and/or cellular Ca2+.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherBlackwell Publishing Asiaen_US
dc.publisher.placeAustraliaen_US
dc.publisher.urihttp://www.blackwell-synergy.com/doi/full/10.1046/j.1440-1681.2003.03814.xen_AU
dc.relation.ispartofpagefrom145en_US
dc.relation.ispartofpageto152en_US
dc.relation.ispartofjournalClinical and Experimental Pharmacology & Physiologyen_US
dc.relation.ispartofvolume30en_US
dc.subject.fieldofresearchcode320699en_US
dc.titlePyruvate-dependent preconditioning and cardioprotection in murine myocardiumen_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.copyrightCopyright 2003 Blackwell Publishing. The definitive version is available at [www.blackwell-synergy.com.]en_AU
gro.date.issued2003
gro.hasfulltextNo Full Text


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