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：BACKGROUND:Stellateganglionblock(SGB)playsaprotectiveroleonthebrain,buttheprecisemecha-nismofactionisnotclear.OBJECTIVE:TosimulateSGBbytransectionofthecervicalsympathetictrunk(TCST)andtoinvestigatetheTCSTeffectsonchangesincerebralinfarctvolumeandoxygenfreeradicallevelsinratswithfocalcere-bralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:AcompleterandomizedcontrolanimalexperimentwasperformedattheInstituteofNeurologicalDiseasesofTaiheHospital,YunyangMedicalCollegefromFebruarytoDecember2005.MATERIALS:Atotalof101healthyWistarrats,weighing280–320g,ofbothgenders,aged17–18weeks,wereusedinthisstudy.2,3,5-triphenyltetrazoliumchloride(TTC)waspurchasedfromChangshaHongyuanBiologicalCompany.Superoxidedismutase(SOD),malondialdehyde(MDA)andnitricoxide(NO)assaykitswereprovidedbyNanjingJianchengBioengineeringInstitute.METHODS:RatswererandomlydividedintoaTCSTgroup,amodelgroupandashamoperationgroup.Successfulmodelswereincludedinthefinalanalysis,withatleast20ratsineachgroup.AfterTCST,ratmodelsoffocalcerebralischemia/reperfusioninjurywereestablishedintheTCSTgroupbyreceivingmiddlecerebralarteryocclusion(MCAO)bytheintraluminalsuturemethodfor2hours,followedby24hoursofreperfusion.Ratmodelsoffocalcerebralischemia/reperfusioninjuryweremadeinthemodelgroup.Ratsintheshamoperationgroupunderwentexperimentalproceduresasforthemodelgroup,threadingdepthof10mm,andmiddlecerebralarterywasnotligated.MAINOUTCOMEMEASURES:BraintissuesectionsoftenratsfromeachgroupwereusedtomeasurecerebralinfarctvolumebyTTCstaining.BraintissuehomogenateofanothertenratsfromeachgroupwasusedtodetectSODactivities,MDAcontentsandNOlevels.Ratneurologicalfunctionwasassessedbyneu-robehavioralmeasures.RESULTS:CerebralinfarctvolumewasbiggerinthemodelgroupthanintheTCSTgr