Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction 英文参考文献.docVIP

Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction 英文参考文献.doc

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Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction 英文参考文献

Meybohmetal.CriticalCare2011,15:R241 /content/15/5/R241 RESEARCH OpenAccess Pharmacologicalpostconditioningwith sevofluraneaftercardiopulmonaryresuscitation reducesmyocardialdysfunction PatrickMeybohm1*,MatthiasGruenewald1,MartinAlbrecht1,ChristinaMüller1,KarinaZitta1,NikolaFoesel1, MoritzMaracke1,SabineTacke2,JürgenSchrezenmeir3,JensScholz1andBertholdBein1 Abstract Introduction:Inthisstudy,wesoughttoexaminewhetherpharmacologicalpostconditioningwithsevoflurane (SEVO)isneuro-andcardioprotectiveinapigmodelofcardiopulmonaryresuscitation. Methods:Twenty-twopigsweresubjectedtocardiacarrest.After8minutesofventricularfibrillationand2 minutesofbasiclifesupport,advancedcardiaclifesupportwasstarted.Aftersuccessfulreturnofspontaneous circulation(N=16),animalswererandomizedtoeither(1)propofol(CONTROL)anesthesiaor(2)SEVOanesthesia for4hours.Neurologicalfunctionwasassessed24hoursafterreturnofspontaneouscirculation.Theeffectson myocardialandcerebraldamage,especiallyoninflammation,apoptosisandtissueremodeling,werestudiedusing cellularandmolecularapproaches. Results:AnimalstreatedwithSEVOhadlowerpeaktroponinTlevels(median[IQR])(CONTROLvsSEVO=0.31pg/ mL[0.2to0.65]vs0.14pg/mL[0.09to0.25];P0.05)andimprovedleftventricularsystolicanddiastolicfunction comparedtotheCONTROLgroup(P0.05).SEVOwasassociatedwithareductioninmyocardialIL-1bprotein concentrations(0.16pg/μgtotalprotein[0.14to0.17]vs0.12pg/μgtotalprotein[0.11to0.14];P0.01),a reductioninapoptosis(increasedprocaspase-3proteinlevels(0.94arbitraryunits[0.86to1.04]vs1.18arbitrary units[1.03to1.28];P0.05),increasedhypoxia-induciblefactor(HIF)-1aproteinexpression(P0.05)and increasedactivityofmatrixmetalloproteinase9(P0.05).SEVOdidnot,however,affectneurologicaldeficitscore orcerebralcellularandmolecularpathways. Conclusions:SEVOreducedmyocardialdamageanddysfunctionaftercardiopulmonaryresuscitationintheearly postresuscitationperiod.Thereductionwasassociatedwithareducedrateofmyocardialproinflammatorycytokine expression,apoptosis,increasedHIF

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