Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane英文文献资料.docVIP

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Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane英文文献资料.doc

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Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane英文文献资料

HindawiPublishingCorporation JournalofAgingResearch Volume2012,ArticleID753949,9pages doi:10.1155/2012/753949 ResearchArticle BlockadeofElectronTransportattheOnsetof ReperfusionDecreasesCardiacInjuryinAgedHeartsby ProtectingtheInnerMitochondrialMembrane QunChen, ThomasRoss, YingHu, 1 1 1andEdwardJ.Lesnefsky1,2,3 1 PauleyHeartCenter,DivisionofCardiology,DepartmentofInternalMedicine,VirginiaCommonwealthUniversity, Richmond,VA23298,USA 2 3 DepartmentofBiochemistry,VirginiaCommonwealthUniversity,Richmond,VA23298,USA CardiologySection,MedicalService111(J),McGuireVAMedicalCenter,Richmond,VA23249,USA CorrespondenceshouldbeaddressedtoEdwardJ.Lesnefsky,ejlesnefsky@ Received12September2011;Revised23November2011;Accepted27December2011 AcademicEditor:PaulaBickford Copyright?2012QunChenetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense, whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited. Myocardialinjuryisincreasedintheagedheartfollowingischemia-reperfusion(ISC-REP)comparedtoadulthearts.Intervention atREPwithischemicpostconditioningdecreasesinjuryintheadultheartbyattenuatingmitochondrialdrivencellinjury.Unfortu- nately,postconditioningisine?ectiveinagedhearts.BlockadeofelectrontransportattheonsetofREPwiththereversibleinhibitor amobarbital(AMO)decreasesinjuryinadulthearts.WetestedifAMOtreatmentatREPprotectstheagedheartviapreservationof mitochondrialintegrity.Bu?er-perfusedelderlyFischer34424mo.ratheartsunderwent25minglobalISCand30minREP.AMO (2.5mM)orvehiclewasgivenfor3minattheonsetofREP.Subsarcolemmal(SSM)andinter?brillar(IFM)mitochondriawere isolatedafterREP.Oxidativephosphorylation(OXPHOS)andmitochondrialinnermembranepotentialweremeasured.AMO treatmentatREPdecreasedcardiacinjury.ComparedtountreatedISC-REP,AMOimprovedinnermembranepotentialinSSM andIFMduringREP,indicatingpreservedinnermembraneintegrity.Thus,directpharmacologicmodulationofelectrontrans- portatREPprotectsm