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