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1、展看IsofluranepreconditioningIschemicbraininjuryisimplicatedinthepathophysiologyofstrokeandbraintrauma,ongthetop10killersintheUSA[1].Manyinterventions,suchasinductionofhypothermiaanduseofglutamatereceptorantagonists,havebeenexploredforpotentialneuroprotectionagainstischemia[2,3].Hoethods
2、toreduceischemicbraininjuryhavenotbeenicpreconditioningisaenoniniainducearobustprotectionagainstthedeleteriouseffectsofsubsequent,prolonged,lethalischemiainmanyorgans,includingbrainandheart[4,5].Earlystudiesshoicpreconditioningoccurredintporalphases:acuteanddelayed[6,7].Theacutephaseis
3、mediatedbyfunctionchangesofexistingproteins,ispresentinutes,anddisappears2-3hourslater[6].Thedelayedphasedevelopshoursafterthepreconditioningevent,requiresneethatpreconditioninginaximallyprotective.Thiseffectatetransporter-dependent[9].Othervolatileanesthetics,suchassevoflurane,halotha
4、neanddesflurane,alsoinducedpreconditioningeffectsinthebrain.Thepotencyofthisprotectioninducedbyvolatileanestheticsiscorrelatedmobility[10].Sinceglutamateaccumulationandthesubsequentglutamatereceptorover-stimulationplayacriticalroleintheischemicbraininjury[11],inedatereceptorover-stimul
5、ation-inducedneuronaldeath.Ourresultsshoulationofthemajorglutamatereceptors[12].Kapinyaetalshouldbecreditedasthefirstgrouptoshoediatedbytheactivationofthemitogen-activatedproteinkinasep38[14].Theisofluranepreconditioning-inducedprotectioninhumanneuroblastomaSH-SY5Ycellsinvolvedtheextra
6、cellularsignal-regulatedkinase-earlygromaturebrains[16].Thisprotectionalsinedatonemonthafterthebrainischemia[17].Insummary,volatileanestheticscaninduceacuteanddelayedphasesofpreconditioningeffectsinthebrain.Sinceisofluraneisarelativelysafeagentandhasbeenfrequentlyusedinpatientsia,these
7、patientsmayhavealreadybenefitedfromitspreconditioningeffects.Studyingthemechanismsofvolatileanestheticpreconditioning-inducedneuroprotectionmayidentifyneicbraininjury.References1.Martin,J.A.,etal.,BirthsandDeaths:PreliminaryDatafor1998.NationalVitalStatisticsReports,1999.47(25):p.1-4
