文档介绍：展看Isofluranepreconditioning
Ischemicbraininjuryisimplicatedinthepathophysiologyofstrokeandbraintrauma,ongthetop10killersintheUSA[1].Manyinterventions,suchasinductionofhypothermiaanduseofglutamatereceptorantagonists,havebeenexploredforpotentialneuroprotectionagainstischemia[2,3].Hoethodstoreduceischemicbraininjuryhavenotbeenicpreconditioningisaenoniniainducearobustprotectionagainstthedeleteriouseffectsofsubsequent,prolonged,ans,includingbrainandheart[4,5].urredintporalphases:acuteanddelayed[6,7].Theacutephaseismediatedbyfunctionchangesofexistingproteins,ispresentinutes,anddisappears2-3hourslater[6].Thedelayedphasedevelopshoursafterthepreconditioningevent,-dependent[9].Othervolatileanesthetics,suchassevoflurane,halothaneanddesflurane,[10].umulationandthesubsequentglutamatereceptorover-stimulationplayacriticalroleintheischemicbraininjury[11],inedatereceptorover-stimulation-[12].
Kapinyaetalshouldbecreditedasthefirstgrouptoshoediatedbytheactivationofthemitogen-activatedproteinkinasep38[14].Theisofluranepreconditioning-inducedprotectioninhumanneuroblastomaSH-SY5Ycellsinvolvedtheextracellularsignal-regulatedkinase-earlygromaturebrains[16].Thisprotectional