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1、Inthisstudy,atransientmechanicalstretchoftheleftventriclesignificantlyreducedinfarctsizeinratheart.AMPKphosphorylationwasenhancedbymechanicalstretchinbothexvivoandinvivo(ACS)heartmodelandwassup-pressedbyGd3+.Mechanicalstretch・inducedcardiopro-tectionwasblockedbyGd3+andCompoundC.AICAR,anAMPKacti
2、vator,insteadofmechanicalstretchprotectedheartfromI/Rinjury.TheseresultssuggestthatAMPKplaysanimportantroleintheSIC,andthisrolemightberegulatedbySACs.Inthisstudy,therewerenosignificantdifferencesinbase-linefunctionalparameters,includingHR,LVEDP,SP,andCBF,amongallgroupspriortoimpartingsustainedi
3、sche-mia(Fig.2CandFig.5C).Therefore,SICcouldnotbeas・Fig.5.Effectsofstretchprecon-ditioningontheinfarctsizeandthefunctionalrecoveryofinvivorathearts・(A)InfarctsizewasmeasuredusingTTCstainingafter30minutesischemiaand1hourreperfusionand(B)normalizedinfarctsizewascal-culatedandcompared.Alldataareme
4、ans±SEMofN>6ineachexperi-mentalgroup.*p<0.05comparedwithI/RCongroup•I/RCon，ischemia-reperfusioncontrol;ACSSham,shaperatedhearts;ACS,aorto・cavalshunt.(C)Functionalrecoveryofinvivostretchedrathearts.Cardiacfunctionwasevaluatedintermsof4parameters;cardiacfunctionalre-covery,Leftventricularend-dias
5、tolicpressure(LVEDP),heartrate,andcoronarybloodflow・Thechangesof4parametersweretracedduring60minutespost-ischemicreperfusionperiod・Alldataaremeans±SEMofN>6ineachexperimentalgroup・*p<0.05comparedwithcontrolgroup.•,ischemia-reperfusioncontrol;o,Sham;▼,10minutesACS;▽,20minutesACS;ACS,aorto-cavalsh
6、unt.cribedtostretchinduced・hemodynamicchanges.Mechanicalstretchintheheartcanbeproducedbyin-creasingtheleftventricularwalltensionexpressedasanincreaseinLVEDP.Inthisstudy,theleftventricularwalltensionwasincreasedbyinvivovolumeoverloadusinganACSratheartmodel.Huangandhiscoworkers[32]demon-stratedtw
7、oepisodesofbriefpressureoverloadoftheleftventriclebytransverseaorticconstrictionsignificantlyducedmyocardialinfarctsize,tAlthoughtheleftventricularsystolicpressurewasraised50%abovethebaselineandtheprotectionofpressureoverloadwasab
