简介：Thephenomenonofischemia/reperfusioninjuryisdescribedintheexperimentalmodelsofacutemyocardialinfarction(AMI),causingadditionalfunctionalandstructuraldamagetotheacutereperfusedmyocardium,andischemicpreconditioningreferstothemyocardialischemiaafteralongperiodofreperfusionbeforeoneorseveralshortoccasionalduplicationofmyocardialischemia/reperfusion1,whichcanincreasemyocardialischemictolerance.ThetherapeuticstrategiesforAMIhavefocusedonmyocardialischemia/reperfusioninjury,whichaccountsforasignificantpartofthefinalinfarctsize.Althoughexperimentsinthelast20yearshavereportedthatpharmacologicalinterventionsatreperfusionmightreducemyocardialreperfusioninjury,thiscouldnotbeconfirmedinhumanstudies.Analternativetochemicalmodifiers,postconditioning(briefrepeatedperiodsofischemiaappliedattheonsetofreperfusion)isanothermethodproventobeefficientinanimalmodelsandtobeconfirmedinrecenthumanstudies.Thissimplemethod,appliedinthefirstminuteofreperfusion,reducesthefinalinfarctsizeby30%-50%.Thisreviewwillfocusonthemechanisms,pharmacologicalpreconditioning,postconditioningtechnique,whichiseasilyapplicableinhumanpatientsinthesettingofAMI.

简介：Objective:Tostudytheeffectofmethylprednisolone(MP)onreperfusioninjuryinsevereuncontrolledhemorrhagicshockandexplorethepossiblemechanisminvolved.Methods:Twelvedogswererandomlydividedintotwogroups,controlgroup(GroupI,n=6)andMPgroup(GroupII,n=6).Theanimalswerebledcontinuouslyfromafemoralarterycathetertoproduceuncontrolledhemorrhagicshockmodels.ResuscitationwithlactatedRinger's(LR)solutionwasinitiatedwhenmeanarterialpressure(MAP)decreasedto20mmHg,andMAPwasmaintainedat30-40mmHg.MP(4mg/kg)wasinjectedintravenouslyinGroupIIwhenresuscitationbegan.WhileinGroupI,normalsaline(NS)wasinjectedinstead.Thelevelsofsuperoxidedismutase(SOD)andmalondialdehyde(MDA)weremeasuredbeforeexsanguination(T1),whenMAPdecreasedto20mmHg(T2),60min(T3)and120min(T4)afterresuscitation.Heartrate,MAPandcardiacoutput(CO)levelswererecordedconcomitantly.Results:InfusionvolumeandhemorrhagevolumeshedfromthesuperiormesentericarteryinGroupIwerehigherthanthoseinGroupII(P<0.01andP<0.05).Afterreperfusion,bloodSODlevelsdecreasedprogressivelyandMDAlevelsincreasedrapidlyinGroupI.InGroupII,bloodSODlevelsatT3andT4decreasedascomparedwiththatatT1butastepwiseincreasewaspresent.AtT4,bloodSODlevelwassignificantlyhigherinGroupIIthaninGroupI(P<0.01).AtT3andT4,MDAlevelsweremarkedlylowerinGroupIIthaninGroupI.Duringreperfusion,MAPwasmoresteadyinGroupIIthaninGroupIandsurvivalrateafter120min(atT4)washigherinGroupIIthaninGroupI(P<0.05).Conclusions:MPhasaprotectiveeffectonsevereuncontrolledhemorrhagicshockandsubsequentreperfusioninjury.Themechanismmainlyinvolvestheanti-lipidperoxidationactivityofMP.

简介：Tostudythechangesofexcitatoryaminoacids(EAAs)andintracellularcalcium([Ca2+]i),andtheprotectiveeffectofEAAsreceptorantagonistsinthetissuesofrabbitlumbarspinalcordafter40-minuesischemiaand4-hoursreperfusion.Methods:Thirtyhealthyrabbitsweredividedintosixgroups:sham-operation,40-minuesischemia,4-hourreperfusion,ketamineandMgSO4treatment,ketaminetreatment,andsalinetreatmentgroups.ThecontentsofEAAs(glutamateandaspartate)and[Ca2+]iweremeasured.Results:Thecontentsofglutamateandaspartateweredecreasedto15.18μmol/g±2.33μmol/gand9.99μmol/g±0.69μmol/g,respectively;13.75μmol/g±2.58μmol/gand6.49μmol/g±1.39umol/gafterreperfusion.Intheischemiagroup,the[Ca2+]iwaselevatedto221.2μg/g±4.27μg/g,andelevatedfurtherto298.3μg/g±9.26μg/gafterreperfusion,beingsignificantlyhigherthanthatofischemiaandcontrolgroups.Ketaminecouldobviouslyincreasethelevelofglutamateandaspartateanddecreasethelevelof[Ca2+]iduringtheischemiaandreperfusioninjury.Conclusions:TheexcitotoxicityofEAAsandtheoverloadofcalciuminducedbyEAAsplayaharmfulroleinischemiaandreperfusioninjury.Ketaminehasaneffectiveinhibitoryeffect.

简介：Objective:Tostudytheprotectiveeffectofischemicpreconditioning(Ⅰ-pre)andischemicpostconditioning(Ⅰ-post)againstischemia/reperfusion(I/R)injuryinrat'sliver.Methods:UsingratmodelofhepaticsegmentalI/Rinjury,ratsweredividedinto5groups:GroupA(shamgroup),GroupB(I/Rinjury),GroupC(Ⅰ-pregroup),GroupD(Ⅰ-postgroup)andGroupE(combinedtreatmentofⅠ-preandⅠ-post).Serumalanineaminotransferase(ALT),aspartateaminotransferase(AST),malondiaidehyde(MDA),glutathione(GSH),superoxidedismutase(SOD),glutathioneperoxidase(GSH-Px)andmyeloperoxidase(MPO)inhepatictissuesweredetermined,respectively.Inaddition,7days'survivalofGroupsB,C,DandEwereevaluated.Results:ComparedwithGroupB,GroupsC,DandEexhibitedsignificantlydecreasedALTandASTrelease,minimizedtissueinjury,suppressedvaluesofMDAandMPO,increasedactivitiesofSOD,GSH-PxandGSH(P<0.05),aswellasimprovedanimalsurvival.ThedifferencesamongGroupsC,DandEwerenotstatisticallysignificant.Conclusions:Ⅰ-pre,Ⅰ-postandcombinedtherapyofⅠ-preandⅠ-posthaveprotectiveeffectagainsthepaticI/Rinjury,whichiscorrelatedwithitsfunctionofreducingtheproductionofreactiveoxygenspecies,maintainingtheactivitiesofantioxidantsystemsandsuppressingneutrophilsrecruitment.NoadditiveeffectcanbeobtainedinGroupE.

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

简介：Brainischemicstrokeistheleadingcauseoflong-lastinginjury,disability,anddeathinadults.Althoughthebrainrepresentsonlyabout2%ofthetotalbodymass,itconsumesalmost20%ofthebody’soxygen.Asaresult,braincellsareextremelysensitivetohypoxia.Oncecerebralischemiaoccurs,thecoreofthe

简介：Ephedrinehasaprotectiveeffectagainstcerebralischemia,butitssideeffectslimititsclinicalapplication.Resultsfromapreviousstudyshowedthat1.5mg/kgperdayephedrinecanpromotemotionrecoveryinratsfollowingcerebralischemia/reperfusionwithoutsignificantsideeffects.Inthepresentstudy,ephedrineatdosesof3.0,2.5and2.0mg/kgwasusedtotreatratswithcerebralischemia/reperfusionandtheeffectsofephedrineontheheart,liver,kidneyandcerebrumwereobserved.Resultsshowedthatthebloodpressureofratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentwaslowerthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion,butthepressuredecreasedwithincreasingdosesofephedrine.Inaddition,serumaspartatetransaminase,alkalinephosphataseandcreatinineconcentrationinratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentweregreaterthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion.Theconcentrationsoftheseenzymesweredecreasedwithincreasingdosesofephedrine.Ephedrine-treatedratsdisplayedhyperemia,degenerationandedemainthecerebrum,liver,heartandkidney.Resultsdemonstratedthatephedrineexhibitedsideeffectsonthecerebrum,heart,liverandkidneyinratsfollowingcerebralischemia/reperfusioninadose-dependentmanner.

简介：AbstractPanax notoginseng is an ancient Chinese medicinal plant that has great clinical value in regulating cardiovascular disease in China. As a single component of panax notoginosides, notoginsenoside R1 (NGR1) belongs to the panaxatriol group. Many reports have demonstrated that NGR1 exerts multiple pharmacological effects in ischemic stroke, myocardial infarction, acute renal injury, and intestinal injury. Here, we outline the available reports on the pharmacological effects of NGR1 in ischemia-reperfusion (I/R) injury. We also discuss the chemistry, composition and molecular mechanism underlying the anti-I/R injury effects of NGR1. NGR1 had significant effects on reducing cerebral infarct size and neurological deficits in cerebral I/R injury, ameliorating the impaired mitochondrial morphology in myocardial I/R injury, decreasing kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin in renal I/R injury and attenuating jejunal mucosal epithelium injury in intestinal I/R injury. The various organ anti-I/R injury effects of NGR1 are mainly through the suppression of oxidative stress, apoptosis, inflammation, endoplasmic reticulum stress and promotion of angiogenesis and neurogenesis. These findings provide a reference basis for future research of NGR1 on I/R injury.

简介：Thisreviewaimsatevaluatingtheexistingevidenceregardingpostreperfusionsyndrome,providingadescriptionofthepathophysiologicmechanismsinvolvedandpossiblemanagementandpreventivestrategies.APubMedsearchwasconductedusingtheMeSHdatabase,＂Reperfusion＂AND＂livertransplantation＂werethecombinedMeSHheadings;EMBASEandtheCochranelibrarywerealsosearchedusingthesameterms.52relevantstudiesandoneongoingtrialwerefound.Theconceptofpostreperfusionsyndromehasevolvedthroughyearstoamultisystemicdisorder.Theimplicationsofthemainorgan,recipientandprocedurerelatedfactorsinthegenesisofthiscomplexsyndromearediscussedinthetextasthenovelpharmacologicandtechnicalapproachestoreduceitsincidence.Howevertheavailableevidenceaboutriskfactors,physiopathologyandpreventivemeasuresisstillconfusing,thepresenceoftwomaindefinitionsandthenumerosityofpossibleconfoundingfactorsgreatlycomplicatestheinterpretationofthestudies.

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简介：瞄准：观察效果是在老鼠肝细胞的cyclinD1表示上的化学家preconditioning在期间早是化学家灌注。方法：54只SD老鼠随机被划分成是preconditioning组(IP)，ischemia/reperfusion组(红外)和假冒的操作组织的化学家(那么)。IP和红外组进一步被划分成四亚群(n=6)。假冒的操作组(那么)担任了控制组(n=6)。部分肝ischemia/reperfusion的一个模型被使用，在哪个老鼠在灌注以前为60min受到肝局部缺血。在IP组的动物经历了在ischemia/reperfusion挑战以前每次为5min是化学家preconditioning两次。在灌注的0，1，2，和4h以后，在每个组的浆液和肝织物被收集检测浆液中高音，肝组织病理学说和cyclinD1mRNA和蛋白质的表示的水平。流动血细胞计数被用来作为房间新生的数量指示物检测房间周期。结果：与红外组相比，IP组在1h显示出显著地更低的中高音水平到4h亚群(P<0.05)。增长索引(PI)由S阶段和G2/M-phase比率显示了[(S+G2/M)/(G0/G1+S+G2/M)]显著地在0和1h在IP组被增加(26.44+/-7.60%对18.56+/-6.40%，41.87+/-7.27%对20.25+/-6.70%，P<0.05)。同时，cyclinD1蛋白质表示能在IP组被检测。但是在红外组，，cyclinD1蛋白质表示发生了在灌注以后的2h。在IP显著地增加的cyclinD1mRNA的表示在0和1h组织(0.568+/-0.112对0.274+/-0.069，0.762+/-0.164对0.348+/-0.093，P<0.05)。结论：局部缺血preconditioning能保护肝细胞免于ischemia/reperfusion损害，它可能早与房间增长和cyclinD1的表示有关在期间是化学家灌注。

简介：目的：探讨局灶性脑缺血再灌注大鼠病理学改变以及针刺的干预作用。方法：采用线栓法建立缺血再灌注模型，应用“醒脑开窍”针法并通过电镜与光镜来观察缺血侧大脑皮层形态结构的变化。结果：脑缺血再灌注可引发大鼠脑神经元、胶质细胞、毛细血管等结构损伤，针剌可改善脑缺血周围区超微结构损伤。并且发现在3h时间点给予针刺干预较其他时间点理想。结论：针刺对局灶性脑缺血再灌注大鼠脑神经细胞超微结构损伤具有保护作用。在3h内给予针刺干预可以收到满意的效果。

简介：ObjectivesTostudytheeffectoflatereperfusiononcaspase-3activityofischemicmyocardiuminrabbitanditssignificance.Methods24adultrabbitswererandomlydividedinto3groups:Sham(S)withoutligationofcoronaryartery,LateReperfusion(LR)withligationfor3hoursfollowingreleasefor3hoursandPersistentIschemia(PI)withpersistentligationofcoronaryarteryfor6hours.Allanimalsweresacrificed6hoursafterthebeginningoftheexperiments.BorderregionofinfarctedmyocardiumwereincisedforanalyzingtheconcentrationofSOD,MDA,GRandtheexpressionofFADD,Caspase-3andtheapoptosisindex(AI).ResultsComparedwiththeShamgroup,LRandPIgroupexhibitedmuchhigherMDA,FADD,Caspase-3,AIandmuchlowerSOD,GR(allP<0.01).ComparedwiththePIgroup,LRgroupexhibitedhigherMDA,FADD,Caspase-3,AIandlowerSOD,GR(allP<0.05).ConclusionsLatereperfusionmarkedlyenhancedtheCaspase-3activityandthenthenumberofapoptoticcardiomyocyteinborderregionofinfractedmyocardium,whichindicatedtheexistenceoflatereperfusioninjury.ThemechanismmayinvolvethehighoxidativestressstateandexpressionofFADD.

简介：NewZealandrabbitswererandomlydividedintoanischemiagroup(occlusionoftheabdominalaortafor60minutes),anischemia-reperfusiongroup(occlusionoftheabdominalaortafor60minutesfollowedby48hoursofreperfusion)andasham-surgerygroup.Two-dimensionalgelelectrophoresisdetected49differentiallyexpressedproteinsinspinalcordtissuefromtheischemiaandischemia/reperfusiongroupsand23ofthemwereidentifiedbymassspectrometry.Intheischemiagroup,theexpressionofeightproteinswasupregulated,andthatoftheremainingfourproteinswasdownregulated.Intheischemia/reperfusiongroup,theexpressionoffourproteinswasupregulated,andthatoftwoproteinswasdownregulated.Inthesham-surgerygroup,onlyoneproteinwasdetected.Intheischemiaandischemia/reperfusiongroups,fourproteinsoverlappedbetweengroupswiththesamedifferentialexpression,includingthreethatwereupregulatedandonedownregulated.Theseproteinswererelatedtoenergymetabolism,celldefense,inflammatorymechanismandcellsignaling.

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简介：ToinvestigateeffectsofShenfuinjectionontheconcentrationsofplasmatumornecrosisfactor-alpha(TNF-α)andinterleukin-6(IL-6),activityofNuclearFactorkappaB(NF.gB)andhearttissueultrastructureduringmyocardialischemia/reperfusion(I/R)injuryinratsanditspotentialmechanism.Methods:Myocardialischemia/reperfusion(I/R)wasproducedbyligationandreleaseoftheleftanteriordescendingcoronaryartery.Ischemialastedfor30minandreperfusionfor60min.Twenty-fourhealthymaleSDratsweighing230-280gwererandomlydividedintothreegroups(n=8,each):GroupⅠ(Sham-operationgroup);GroupⅡ(I/Rgroup);GroupⅢ(Shenfugroup),inwhichShenfuinjection(10ml/kg)wasintraperitoneallyinjected30minbeforeischemiainanimalswithI/R.TheplasmaconcentrationsofIL-6andTNF-αweremeasuredbyELISA,andtheheartwasharvestedfordeterminationofNF-κBlevelsbyEcl-westernblotanalysis.Electronmicroscopywasusedtostudyitsultrastructure.Results:Afterreperfusion,NF-κBbindingactivityinmyocardialnucleiandtheplasmaconcentrationsofIL-6andTNF-αweresignificantlyincreasedinGroupⅡ,comparedwithGroupⅠ(P<0.01),andtheyweremarkedlyreducedinGroupⅢ,comparedwithGroupⅡ(P<0.01).Inaddition,electronmicroscopicexaminationshowedmoreseriousinjuryofthemyocardiumultrastructureinGroupⅡ,whileinGroupⅢthemyocardialultrastructurewassimilartonormalstate.Conclusions:ShenfuinjectioninhibitsNF-κBactivityinI/Rmyocardiumandleadstodown-regulationofproinflammatorycytokineexpression,whichmightbeoneofthemolecularmechanismsofShenfuinjectionincardioprotection.

简介：客观：在兔子在针的绳索ischemia/reperfusion(I/R)以后在lipidperoxidation和apoptosis上学习白果树biloba摘录(GBE)的效果。方法：SpinalcordI/R损害模型根据对Erten等的描述被建立。27只NewZealand白兔子的一个总数随机被划分成三个组：一个假冒的组(9只兔子对待withs火腿操作但是没有大动脉的吸藏)，一个模型组(与大动脉的吸藏对待的9只兔子并且匹配卷盐)，并且一个GBE组(与大动脉的吸藏andGinaton(100mg/kg)对待的9只兔子在大动脉的夹钳前并且在灌注的发作注射了30分钟)。Theneurological结果分别地在灌注以后在24和48个小时被评估。针的绳索malondialdehyde(MDA)水平，超级氧化物dismutase(草皮)然后被检测。神经cellapoptosis被终端deoxynucleotidyltransferase(TdT)决定标记的-mediateddUTP-fluorescence刻痕结束(TUNEL)方法和bcl-2和bax的表示是examinedhistologically在有免疫组织化学的针的绳索。结果：I/Rproduced在神经病学的得分的重要减少。GBE组的马达分数比在在灌注以后的24和48个小时的模型组的那些显著地高(P<0.05)。与模型组相比，GBE改善了草皮的下面规定并且生产了MDA水平的重要减小(P<0.01)。为在模型组的TUNEL的积极房间是多于GBE组的那些的大部分(P<0.01)。bcl-2在I/R以后是起来调整的，特别在theGBE组(P<0.01)。bax的起来规定被GBE极大地减少(P<0.01).Conclusions：GBE对针的绳索I/R损害，和机制有保护的效果可以是它能清除氧释放激进分子并且禁止神经房间的apoptosis。

简介：AbstractMitochondrial injury and endoplasmic reticulum (ER) stress are considered to be the key mechanisms of renal ischemia-reperfusion (I/R) injury. Mitochondria are membrane-bound organelles that form close physical contact with a specific domain of the ER, known as mitochondrial-associated membranes. The close physical contact between them is mainly restrained by ER-mitochondria tethering complexes, which can play an important role in mitochondrial damage, ER stress, lipid homeostasis, and cell death. Several ER-mitochondria tethering complex components are involved in the process of renal I/R injury. A better understanding of the physical and functional interaction between ER and mitochondria is helpful to further clarify the mechanism of renal I/R injury and provide potential therapeutic targets. In this review, we aim to describe the structure of the tethering complex and elucidate its pivotal role in renal I/R injury by summarizing its role in many important mechanisms, such as mitophagy, mitochondrial fission, mitochondrial fusion, apoptosis and necrosis, ER stress, mitochondrial substance transport, and lipid metabolism.

简介：BACKGROUND:RecentstudieshavesuggestedthatmitochondrialATP-sensitiveK+channelopenerscouldreducemyocardiuminfarctsize,andprotectthefunctionofthemitochondria.OBJECTIVE:ToinvestigatethechangesofcerebralinfarctionvolumeandtheactivityofmarkerenzymesinbrainmitochondriaofratsgiventheATP-sensitiveK+channelopener,nicorandil,beforefocalcerebralischemia/reperfusion(I/R).DESIGN,TIMEANDSETTING:Randomized,controlledanimalexperiment,completedattheBrainScientificResearchCenteroftheAffiliatedHospitalofQingdaoUniversityfromJulytoNovember2007.MATERIALS:SixtyhealthymaleWistarratsweighing280–300g.Nicorandil,5-hydroxydecanoate(5-HD)andcytochromeCwerepurchasedfromSigmaintheUSA.Standardmalondialdehyde(MDA)andproteinwerepurchasedfromNanjingJianchengBiotechnologyInstitute.METHODS:Sixtyratswererandomlydividedintoashamoperationgroup,amiddlecerebralarteryocclusion(MCAO)group,anicorandilgroupandanicorandil+5-HDgroup.MCAOfor2hourswasperformedintheMCAOgroup,nicorandilgroupandnicorandil+5-HDgroup.Atotalof5mLsalineweregiventotheMCAOgroupbeforeMCAO.ThenicorandilgroupwasinjectedwiththeATP-sensitiveK+channelopenernicorandil10mg/kgintraperitoneally30minutesbeforeMCAO.Thenicorandil+5-HDgroupwasinjectedwith5-HD10mg/kgintravenously15minutesbeforethesametreatmentasthenicorandilgroup.MAINOUTCOMEMEASURES:Infarctvolumebytotalbrainslicecalculation,activitiesofsuccinatedehydrogenase(SDH)andcytochromeoxidase(CO),andcontentofMDAwereobservedat22hoursofreperfusionafter2hoursMCAO.RESULTS:Sixtyratswereincludedinthefinalanalysis,withoutanyloss.(1)Infarctvolume:comparedwiththeMCAOgroupandnicorandil+5-HDgroup,thepercentageofinfarctvolumewassignificantlydecreasedinthenicorandilgroup(P<0.01).(2)ThecontentofMDA,expressionofSDHandCOinbrain:theexpressionsofSDHandCOintheshamop

简介：Objective:Toinvestigatetheunderlyingneurobiologicalmechanismoftheprotectiveeffectofelectroacupuncture(EA)duringcerebralischemia-reperfusion(CI-R).Methods:Inthefirstpartofthestudy,15SDratswereevenlyrandomizedintocontrolgroup,CI-R-48hmodelgroupandCI-R-48h+EAgroup.ThecorticalapoptosisandexpressionofBcl-2andBaxproteinsineachgroupweredetectedbyflowcytometer(FCM).Inthesecondpartofthestudy,75SDratswereevenlyrandomizedintocontrol,CI-R-3min,CI-R-3min+EA,CI-R-48handCI-R-48h+EAgroups.Corticalnorepinephrine(NE)concentrationwasdetectedbyfluorescencespectrometer.CI-Rmodelwasestablishedbyocclusionofthebilateralcommoncarotidarteriesandreperfusion.EA(4～16Hz,1～3V)wasappliedafterreperfusionrespectively.Results:Inthefirstpartofthisstudy,resultsindicatedthatthenumberoftheapoptoticneuronsandtheapoptosisrateofCI-R-48hgroupweresignificantlyhigherthanthoseofcontrolgroup;whilecomparisonbetweenCI-R-48h+EAandCI-R-48hgroupsshowedthatthenumberoftheapoptoticneuronsandtheapoptosisrateoftheformergroupweresignificantlylowerthanthoseofthelatergroup(P<0.05).Incomparisonwithcontrolgroup,afterCI-48h,Baxexpressionwasup-regulatedsignificantlyandBcl-2down-regulatedmarkedly(P<0.05).ComparisonbetweenCI-R-48handCI-R-48h+EAgroupindicatedthatBaxexpressionofthelatergroupwassignificantlylowerthanthatoftheformergroup,whileBcl-2expressionofCI-R-48h+EAgroupwassignificantlyhigherthanthatofCI-R-48hgroup(P<0.05),suggestingthatEAcouldreverseCIinducedreactionsofthesetwoindexes.Inthesecondpartofthestudy,incomparisonwithcontrolgroup,NEconcentrationincerebralcortexofCI-R-3mingroupincreasedsignificantly(P<0.05);whileNEcontentofCI-R-3min+EAgroupwassignificantlylowerthanthatofCI-R-3mingroup(P<0.05).NosignificantdifferencewasfoundbetweenCI-R-3mingroupandcontrolgroupincorticalNEl