简介：Thephenomenonofischemia/reperfusioninjuryisdescribedintheexperimentalmodelsofacutemyocardialinfarction(AMI),causingadditionalfunctionalandstructuraldamagetotheacutereperfusedmyocardium,andischemicpreconditioningreferstothemyocardialischemiaafteralongperiodofreperfusionbeforeoneorseveralshortoccasionalduplicationofmyocardialischemia/reperfusion1,whichcanincreasemyocardialischemictolerance.ThetherapeuticstrategiesforAMIhavefocusedonmyocardialischemia/reperfusioninjury,whichaccountsforasignificantpartofthefinalinfarctsize.Althoughexperimentsinthelast20yearshavereportedthatpharmacologicalinterventionsatreperfusionmightreducemyocardialreperfusioninjury,thiscouldnotbeconfirmedinhumanstudies.Analternativetochemicalmodifiers,postconditioning(briefrepeatedperiodsofischemiaappliedattheonsetofreperfusion)isanothermethodproventobeefficientinanimalmodelsandtobeconfirmedinrecenthumanstudies.Thissimplemethod,appliedinthefirstminuteofreperfusion,reducesthefinalinfarctsizeby30%-50%.Thisreviewwillfocusonthemechanisms,pharmacologicalpreconditioning,postconditioningtechnique,whichiseasilyapplicableinhumanpatientsinthesettingofAMI.

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

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简介：backgroundIt'sestablishedthatAngiotensinⅡanditsreceptorsareinvolvedinintimalhyperplasiaafterballooninjuryandstentrestenosis.Recentevidencealsosuggeststhatstatinshavesomeanti-intimalhyperplasiaeffects.Inthisstudy,theeffectofRosuvastatinonexpressionofangiotensinⅡreceptorsinrataorticendotheliumafterballooninjuryisthereforeinvestigated.MethodsAll52WistarKyotoratswereestablishedtoaortainjurymodelsby2Fballooncatheter,thenwererandomlydividedintoshamoperationgroup,aortainjurygroupandRosuvastatin-treatmentgroup.After14days,theaorticspecimensoftheanimalswereharvestedandperformedimmunohistochemistryanddeterminationofmolecularbiology.ResultsTheresultsshowedthat(i)The14days-ballooninjuryinducedobviousintimathickening(P<0.01),however,thephenomenonwasreducedby14days-treatmentwithRosuvastatin(P<0.01).(ii)TheexpressionsofangiotentionⅡtypeⅠ(AT1)andtypeⅡ(AT2)receptormRNAandproteinweremarkedlyup-regulatedbytheballooninjury(P<0.01),after14days-treatmentwithRosuvastatin,theexpressionofAT1receptormRNAanditsproteinwasdecreased(P<0.01),buttheexpressionofAT2receptormRNAanditsproteinwasfurtherincreased(P<0.05).ConclusionInthisstudy,weobservedthattheballooninjuryinduced-intimathickeningwasreducedbyRosuvastatininrats,whichmightbelinkedwiththeregulationofexpressionofangiotensinⅡreceptors.

简介：ObjectivesInvestigatedtheeardioproteetiveandmechanismsoflosartanonwholeisolatedisehemiereperfusedratheart.MethodsLangendorffperfusedsystemswasusedtoinvestigatelosartaneffectonwholeisolatedratheartsinCPK,LDH,MDA,SOD,angⅡandarrhythmia.ResuitsLosartandecreasedincidenceofarrhythmia,improvedatrialventrieularblockrecoveryinreperfusionperiod,duringisehemieperiod,CPKandLDHinI/Rgroupincreasedsignificantlycomparedwithcontrolgroup,51.33±27.02vs22.42±13.33,31.80±4.56vs22.28±15.96,respectively,butgreatlydecreasedinlosartangroupcomparedwithI/Rgroup,23.90±21.74vs51.33±27.02and11.50±13.20vs31.80±4.56,respectively.DuringreperfusionperiodCPK,LDHincreasedsignificantlyinI/Rgroupcomparedwithcontrolgroup,49.11±20.63vs12.14±5.92and28.70±4.69vs23.10±21.38,respectively,butdecreasedgreatlyinlosartangroupcomparedwithI/Rgroup,39.40±9.60vs49.11±20.63and14.50±13.75vs28.70±4.69.ThecontentofMDA,angIIinI/Rgroupmyoeytesishigherthancontrolgroup's,26.±9.25vs17.2±3.37and8.43±3.81vs4.80±0.20.HoweverthecontentofSODintwogroupshasnosignificantlychange,148.20±8.72vs145.08±6.82.thecontentofMDAinlosartangroupmyocardialtissueismuchlowerthancontrolgroup,15.92±4.05vs26.80±9.25andthecontentofangⅡinlosartangroupmyocardialtissueismuchhigherthanI/Rgroup,12.44±6.09vs8.43±3.21.ThedepartmentofcardiologyofsecondhospitalofTianjinmedicaluniversityTianjin300211However,SODhasnosignificantchangeintwogroups,143.47±7.91vs145.08±6.82.ConclusionsLosartanagainstisehemie-reperfusioninjuryofwholeisolatedrathearts,thosebeneficialeffectsaremediateprimarilybytheinhibitedofangiotensinⅡbindingwithitsreceptorandinhibitedoxygenfreeradicalscavengingpotential.

简介：BackgroundIntravascularvolumeexpansionrepresentsabeneficialmeasureagainstcontrast-inducedacutekidneyinjury(CI-AKI)inpatientsundergoingelectiveangiographicprocedures.However,theefficacyofthispreventivestrategyhasnotyetbeenestablishedforpatientswithST-elevation-myocardialinfarction(STEMI),whoareathigherriskofthiscomplicationafterprimarypercutaneouscoronaryintervention(PCI).Inthisrandomizedstudyweinvestigatedthepossiblebeneficialroleofperiproceduralintravenousvolumeexpansionandwecomparedtheefficacyof2differenthydrationstrategiesinpatientswithSTEMIundergoingprimaryPCI.MethodsandResultsWerandomlyassigned450STEMIpatientstoreceive(1)preprocedureandpostprocedurehydrationofsodiumbicarbonate(earlyhydrationgroup),(2)postprocedurehydrationofisotonicsaline(latehydrationgroup),or(3)nohydration(controlgroup).TheprimaryendpointwasthedevelopmentofCI-AKI,definedasanincreaseinserumcreatinineof≥25%or0.5mg/dLoverthebaselinevaluewithin3daysafteradministrationofthecontrastmedium.Moreover,weevaluatedapossiblerelationshipbetweentheoccurrenceofCI-AKIandtotalhydrationvolumeadministered.Therewerenosignificantdifferencesinbaselineclinical,biochemical,andproceduralcharacteristicsinthe3groups.Overall,CI-AKIoccurredin93patients(20.6%):theincidencewassignificantlylowerintheearlyhydrationgroup(12%)withrespecttoboththelatehydrationgroup(22.7%)andthecontrolgroup(27.3%)(Pfortrend=0.001).Inhydratedpatients(earlyandlatehydrationgroups),lowerinfusedvolumeswereassociatedwithasignificantincreaseinCI-AKIincidence,andtheoptimalcutoffpointofhydrationvolumethatbestdiscriminatespatientsathigherriskwas≤960mL.ConclusionsAdequateintravenousvolumeexpansionmaypreventCI-AKIinpatientsundergoingprimaryPCI.Aregimenofpreprocedureandpostprocedurehydrationtherapywithsodiumbicarbonatea

简介：ObjectivesNitroglycerine(NTG)enhancescoronarybloodflowtocompromisedmyocardiumisimportantinrelievingischemia.However,themechanismforthisincreaseinmyocardialbloodflow(MBF)isnotwelldefined.Insmallvesselsandcapillaries,relativebloodviscosityplaysaveryimportantroleindeterminingmyocardialvascularresistance(MVR).MVRreduceisduepartlytotheincreaseinnegativechargeoferythrocytesurface.WethereforehypothesizedthattheenhancementofnutrientbloodflowtozonesofmyocardialischemiaduringNTGispartlysecondarytoreducedMVRandbloodflowviscosity.Thelatterisaffectedbythenegativechargeoferythrocytesurface.Methods6dogswithLADflow-limitingstenosis(group1)and6dogswithLADflow-limitingstenosisandLCxoccmusion(group2)werestudied.AtbaselineandduringintracoronaryinfusionsofNTG(0.3-0.6μg·kg-1·min-1),hemodynamics,MBF(mL·min-1·g-1),wholebloodviscosity(WBη,mPa.S),elongationindex(EI),eletrophoreticmobilityoferythocytes(EME,[μ.s-1)/(V.cm-1)])andpercentwallthickening(%WT)weredetermined.MVRwascalculatedusingdrivingpressure/MBF.ResultsAscomparedtobaseline,nochangesinhemodynamicswereseenduringNTG.MBFincreasedandMVRdecreasedsignificantlyinnormalbed,thecentral25%andtheentireofstenosedbed(P<0.05),withadecreaseinWBηinbothgroup1andgroup2dogs(18.6±9.7%and19.2±14.5%,respectively).However,the%decreaseinWBηwasproportionedtothe%increaseinMBForthe%decreaseinMVRonlyinthecentral25%ofstenosedbed(r=0.87,P<0.001),butnotintheentirestenosedbedandnormalbed.EIdidnotshowstatisticallysignificantdifferencesbetweenduringNTGandatbaseline,butEMEdidincrease.Andthe%decreaseinWBηduringNTGwasrelatedtothe%increaseinEME(r=0.83,P=0.01).ConclusionsNTGreducedmyocardialvascularresistanceandbloodviscosityduetothechangeofnegativechargeoferythrocytesurfacemay,inpart,bethe

简介：ObjectivesTheeffectsofcarvediloloncalciumcurrent(ICa)wereinvestigatedinisolatedadultratventricularmyocytes.MethodsICawasrecordedbyusingwhole-cellpatch-clamprecordingtechnique.ResultsCarvedilolreversiblyinhibitedICainaconcentration-dependentmanner,carvedilolat0.1,0.3,1and10μmol/LintheextracellularsolutiondecreasedpeakICaby1.52%,18.04%,37.34%and72.18%,respectively.Thesteady-stateinactivationcurveofICawasshiftedtomorenegativepotentials,whiletheactivationcurvewasnotaltered.Therecoveryfrominactivationwasshiftedtorightdirection,itcouldnotberecoveredcompletely.Inaddition,Pretreatmentofventricularmyocyteswithprazosinandpropranololcouldn'tblockthecarvedilol-inducedreductionofICa.ConclusionsCarvedilolinhibitsICainadultratventricularmyocytesbymechanismsinvolvingpreferentialinteractionwiththeinactivatedstateofcalciumchannel.