简介：BackgroundMyocardialfibrosisisoneprocessofthevariousheartdiseases,whichleadstocommonpathologicalchangeswhenitdevelopstoacertainstage.Itisthemaincauseofventricularremodelingwhicheventuallyleadstodifferentdegreesofcardiacdysfunction,malignantarrhythmiasandsuddencardiacdeath.Manystudieshaveshownthatvariouscytokinesplayaveryimportantroleinthedevelopmentofmyocardialfibrosis.Thispaperreviewsthelatestresearchesontheroleofcytokinesinmyocardialfibrosis.

简介：ObjectivesToinvestigatetheprotectiveeffectofthrombopoietin(TPO)onmyocardialcellsinvitro.MethodsH9C2celllinewasmaintainedinIscove’smodifiedDulbecco’smedium(IMDM)supplementedwith10%calfserum.Beatingcellsfromheartventriclesofneonatalheartwereculturedataninvitrosystem.Apoptosisofthecelllineabovewasinducedbytreatmentofdoxorubicin(DOX)andwasblockedbyTPO.CellsurvivalrateofH9C2cellwasmeasuredbytheMTTassay.Changesofbeatingrateofneonatalmyocardialcellswerecapturedbydigitalcameraandbeatingratewascalculated.Flowcytometrywasemployedtostudyanti-apoptoticeffectofTPObystainingJC-1proteintoH9C2cell.ResultsMTTassaydemonstratedthatdoxorubicinreducedcellsurvivalrateby73.8%±1.1%,50ng·mL-1and100ng·mL-1TPOincreasedcellsurvivalrateby84.6%±3.6%(P<0.05),86%±4%(P<0.01)atadose-dependentmanner.Beatingrateofprimaryneonatalmyocardialcellsalsodecreasedto15%±8%at48h,100ng·mL-1TPOimprovedbeatingrateto48%±11%(P<0.01).TPOdecreasedapoptoticratefrom19%±9%to11%±6%(P<0.05).ConclusionsTPOhasprotectiveeffectonmyocardialcellsinvitro.Anti-apoptosisisoneofthemechanismsbywhichTPOprotectsinjuredheart.

简介：BackgroundStatinsreduceadversecardiovascularoutcomesandslowtheprogressionofcoronaryatherosclerosisinproportiontotheirabilitytoreducelow-densitylipoprotein(LDL)cholesterol.However,fewstudieshaveeitherassessedtheabilityofintensivestatintreatmentstoachievediseaseregressionorcomparedalternativeapproachestomaximalstatinadministration.MethodsWeperformedserialintravascularultrasonographyin1039patientswithcoronarydisease,atbaselineandafter104weeksoftreatmentwitheitheratorvastatin,80mgdaily,orrosuvastatin,40mgdaily,tocomparetheeffectofthesetwointensivestatinregimensontheprogressionofcoronaryatherosclerosis,aswellastoassesstheirsafetyandside-effectprofiles.ResultsAfter104weeksoftherapy,therosuvastatingrouphadlowerlevelsofLDLcholesterolthantheatorvastatingroup(62.6vs.70.2mgperdeciliter[1.62vs.1.82mmolperliter],P<0.001),andhigherlevelsofhigh-densitylipoprotein(HDL)cholesterol(50.4vs.48.6mgperdeciliter[1.30vs.1.26mmolperliter],P=0.01).Theprimaryefficacyendpoint,percentatheromavolume(PAV),decreasedby0.99%(95%confidenceinterval[CI],1.19to-0.63)withatorvastatinandby1.22%(95%CI,-1.52to-0.90)withrosuvastatin(P=0.17).Theeffectonthesecondaryefficacyendpoint,normalizedtotalatheromavolume(TAV),wasmorefavorablewithrosuvastatinthanwithatorvastatin:-6.39mm3(95%CI,-7.52to-5.12),ascomparedwith?4.42mm3(95%CI,-5.98to-3.26)(P=0.01).Bothagentsinducedregressioninthemajorityofpatients:63.2%withatorvastatinand68.5%withrosuvastatinforPAV(P=0.07)and64.7%and71.3%,respectively,forTAV(P=0.02).Bothagentshadacceptableside-effectprofiles,withalowincidenceoflaboratoryabnor-malitiesandcardiovascularevents.ConclusionsMaximaldosesofrosuvastatinandatorvastatinresultedinsignificantregressionofcoronaryatherosclerosis.DespitethelowerlevelofLDLcholesterolandthehi

简介：BackgroundAlthoughalotofstudieshavebeenperformedonthelongtermoutcomeinadultswithrepairedtetralogyofFallot(TOF)indevelopedcountries,butrareinformationforprimarycorrectionofadultTOFisavailable.Theresearchfocusingontheeffectoftransanularpatch(TAP)forprimarycorrectionofTOFinadulthoodisstillabsent.Viaretrogradeanalysisof7-yearfollow-up,thisstudywasdesignedtoexploretheeffectofthetransanularpatchforprimarycorrectioninadultTOFonthesurgicaloutcome,postoperativecardiacfunctionandmorbidity,aswellastoaddressthemanagementofthecomplication.MethodsAtotalof151consecutiveadultpatients(age≥18)whounderwentprimaryradicalcorrectionofTOFform2007-2014wereselectedanddividedintoTAPandnon-TAPgroupsbasedontheEACTSdatabase.Resultsofdemographicstatisticcharacteristics,echocardiography,color-Dopplerechocardiography,cardiovascularenhancedcontrastcomputedtomography(CT),and/orcardiaccatheterization;intraoperativeinformation,postoperativeresultsandoutcomeswerereported.Duringfollow-up,shorttermwasdefinedwithin3monthsafterdischarge,andmidtermwasdefinedas6-12monthsafterdischarge.ResultsTotalpostoperativemortalitywas5.96%inallthecases,6.96%inTAPgroup,and2.78%(1/36)innon-TAPgroup.Therewasnosignificantdifferencebetweentwogroups.Follow-upperiodrangedfrom3monthsto62months.Readmissionoccurredandwasfollowedbymedicaltreatmentwithoutre-dosurgeryin6cases(3.97%).TheshorttermechocardiographydemonstratedthatpulmonaryregurgitationandshorttermtricuspidregurgitationafterdischargeinTAPgroupweremoresevere(P<0.001).Theshorttermresidualpulmonarystenosis(RVOTO)severityafterdischargeinTAPgroupwaslesssevere(P=0.018).MidtermechocardiographyafterdischargedemonstratedpulmonaryregurgitationandtricuspidregurgitationinTAPgroupwerestillmoresevere(P=0.003).TheseverityofresidualpulmonarystenosisinT

简介：ObjectivesToexploretheeffectoflosartanoncardiacandrenalfunctioninpatientswithchronicheartfailure(CHF).MethodsSixty-fivepatientswithCHFweredividedintotwogroupsusingarandomized,controlandsingleblindmethod:losartangroup(n=30)andconventiongroup(n=35),withatreatmentcourseof8weeksforbothgroups.TheconcentrationsofcystatinC(cysC)inserum,microamountalbumin(MA)inurineweremeasuredbyimmunoturbidimetry.Theconcentrationofaquaporin-2(AQP-2)wasdeterminedbyenzyme-linked-immunosorbentassay(ELISA)andtheheartcontractilefunctionwasmeasuredbyechocardiographybeforeandaftertreatmentrespectively.ResultsComparingwithroutinetreatmentgroup,leftventricularend-diastolicdimension(LVEDd)decreasedsignificantly,whileleftventricularejectionfraction(LVEF)andleftventricularfractionalshortening(LVFS)increasedsignificantlyinlosartangroup.ThelevelsofcysCinserumandMA,AQP-2inurineweresignificantlylowerinlosartangroupthaninroutinetreatmentgroup.ConclusionLosartancanimprovecardiacandrenalfunctioninpatientswithCHF.

简介：Toevaluatetheeffectofatrovastatintherapyonborderlinevulnerablelesionsinpatientswithacutecoronarysyndrome(ACS).MethodsPatientswithACSunderwentcoronaryangiography(CAG)andintravascularultrasound(IVUS)investigation.Patientswithculpritvulnerableborderlinelesionswereenrolled.Nocoronaryinter-ventionwasperformedontheselesions.Allthepatientsreceivedatrovastatintherapyfor12monthsandunderwentclin-icalfollow-upalongwithIVUSfollow-up.Crosssectionarea(CSA)ofthetargetedlesion,CSAofthereferencearter-ies(extraelasticmembrane),minimallumenCSA,andplaqueareaweremeasuredatbaselineandfollow-ups.Ad-verseeventsincludedrecurrentangina,recurrentmyocardialinfarction,revascularizationanddeath.ResultsNoad-verseeventswasreportedduringfollow-upperiod.Comparedwithbaselinedata,thelevelofApoBdecreasedsignifi-cantlyattheendofthestudy(0.589±0.136g/Lvs0.681±0.132g/L,P=0.03).Boththepercentdiametersteno-sisandthepercentareastenosisdetectedbyCAGdisplayedminimalchange((62.50±10.21)%vs(54.79±12.35)%,P=0.48and(58.61±8.36)%vs(48.18+10.56)%,P=0.78).DetectedbyIVUS,theminimallu-minalCSAofthetargetedlesionincreasedsignificantly(6.32±2.42mm2vs5.63±2.51mm2,P<0.01),theplaqueareaandCSAstenosisdecreased(7.70±2.19mm2vs8.17±2.55mm2,P<0.05and56.94±8.47%vs61.4±110.34%,P<0.01).Atotalof25softplaques(50%)transformedintofibrousplaque.ConclusionsAtro-vastatintherapystabilizesborderlinevulnerableplaqueandreversesatherosclerosisprogressioninpatientswithACS.

简介：ObjectivesTostudythedepressiveeffectoftheantisenseoligonuceotides(ASODN)ofc-mycandproliferatingcellnuclearantigen(PCNA)ontheproliferationofVSMC.MethodsTakingtheVSMCobtainedfromrataortathoracaliscultured4～8generationasresearchobject.Theobjectsweredividedintothreegroupstocarryoutcontrolstudy:controlgroup,PCNAASODNgroupandc-mycASODNgroup.TheASODNs'workingconcentrationallwere1:50.ThedepressiveeffectofASODNonVSMCproliferationwasinvestigatedbycellcounting,MTTand3H-TdRincorporationassay;PCNAandc-mycexpressionweredetectedbyimmunohistochemicalmethodaftertransferringPCNAandc-mycASODNintoVSMC.ResultsPCNAandc-mycASODNcouldinhibittheproliferationofVSMCsignificantly,comparedwithcontrolgroup(P<0.05).②TransferringPCNAandc-mycASODNintoVSMCobtainedsuccessfully;thecorrespondinggenewasinhibitedobviously;comparedwithcontrolgroup(P<0.05).ConclusionsPCNAandc-mycmightplayaconsiderableroleintheVSMCproliferationprocess.ThecorrespondinggenecouldbedepressedsuccessfullyaftertransferringPCNAandc-mycASODNintoVSMC,andthentheproliferationofVSMCwassloweddown.Thisstudypresentedabeneficialproposalandtheoreticalfundamentforatherosclerotictreatment.

简介：ObjectivesToinvestigatetheeffectoftelmisartanonhumanumbilicalveinendothelialcells(HUVEC)exposedtohighglucoseinvitroandtherelatedmechanism.MethodsHUVECswereincubatedwithtelmisartanandglucose(5mmol/L,30mmol/L)at0h,12h,24h,36h,48h,respectively.Thelevelofmalondialdehyde(MDA)andsuperoxidedismutase(SOD)inthesupernatantofculturedendothelialcellswasmeasuredbythiobarbituricacidtestandxanthineoxidasetest.TheexpressionofPPAR-γwasdeterminedat24hourwithWesternblottechnique.ResultsWhentheendothelialcellswereculturedinhighglucoseenvironment,theMDAlevelwassignificantlyincreased,buttheSODactivityandtheproteinexpressionofPPAR-γweremarkedlydecreased.However,thehighglucose-inducedeffectswereinhibitedbytelmisartanintervention.ConclusionTelmisartancandecreaseoxidativestressandincreasePPAR-γexpressionofendothelialcellsinhighglucoseenvironment.

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.

简介：backgroundStudiesshowedthatarterialelasticitychangesappearearlierthananystructuralchanges,therefore,itsaccurateevaluationcouldbeappliedatearlystagetopreventdisease.Echo-tracking(E-tracking)techniquecantrackthewallmotiontrajectoryinreal-time,calculatethechangeinvasculardiameterautomatically,andassessmentofvascularstiffnessandflexibilitydirectly.Thisarticleaimstoassessthechangeofelasticityofcarotidarteryafterhormonetherapy(HT)usingEcho-trackingtechnology.MethodsEcho-trackingwasusedtoevaluatethecarotidelasticmoduli,suchasthepressure-strainelasticmodulus(Eρ),stiffnessparameter(β),arterialcompliance(AC),pulsewaveconductingvelocity(PWVβ)andaugmentationindex(AI)byAlokaα10colorDopplerultrasounddiagnosissystem.ResultsEρ,βandPWVβinHTgroupweresignificantlylowerthanthoseinthecontrolgroup(P<0.01),whileACwasobviouslyhigherthanthecontrolgroup(P<0.01).E2wasnegativelyrelatedtoβ,EρandPWVβ(r=-0.607,r=-0.573,r=-0.574,P<0.001),whilepositivelyrelatedtoAC(r=0.574,P<0.001);endothelial-dependentdilatation(EDD)wasnegativelyrelatedtoβ,EρandPWVβ(r=-0.521,r=-0.411,r=-0.456,P<0.001),whilepositivelyrelatedtoAC(r=0.443,P<0.001);ButIMTwaspositivelyrelatedtoβ,EρandPWVβ(r=0.553,r=0.444,r=0.529,P<0.001),whilenegativelyrelatedtoAC(r=-0.400,P<0.001).ConclusionsArterialstiffnessincreasesandcompliancedecreasesinmenopausalwomen.AsEDDdecreasesarterialelasticityrecedes,andHTcanimprovearterialelasticity.E-trackingtechnologycandiscovertheearlychangesinarterialstiffnesseffectivelyanditismoresensitiveinfindingoutthechangesofstiffnessinearlyatherosclerosisthanIMTofcarotidartery.

简介：Carvedilol,nonselectiveβ-adrenoreceptorantagonist,wasshowedprotectiveeffectsagainstacutemyocardialinfarction(AMI)-inducedmyocardialinjury,however,themechanismsunderlyingtheantifibrosiseffectofcarvedilolhasnotbeenwellknown.Theaimofthepresentstudywastoinvestigatethepotentialmechanismfortheanti-fibrosiseffectofcarvedilolagainstAMI-inducedmyocardialfibrosisinrats.MethodsMaleSDratswererandomizedintotheshamgroup,LADsurgery-AMImodelgroup,AMIpluslowdoseofcarvediloltreatmentgroup(1mg/kgperday,CAR-L),AMIplusmediumdoseofcarvediloltreatmentgroup(5mg/kgperday,CAR-M)andAMIplushighdoseofcarvediloltreatmentgroup(10mg/kgperday,CAR-H).Thepassage3neonatalSDratcardiacfibroblastswereusedforhypoxia/normoxia(2h/4h)treatmentinthepresenceofcarvedilol(0,1,2and4μM).ResultsCardiacremodelingandimpairedheartfunctionwereobservedafter14-weekLADsurgerytreatment,however,andthecardiacremodelinganddecreasedejectionfraction(EF%)andfractionalshortening(FS%)wereefficientlyrescuedintheCAR-MandCAR-Hgroups.Theup-regulatedexpressionsofCol1a1,Col3a1andα-SMAatmRNAandproteinlevelsweresignificantlyreducedintheCAR-MandCAR-Hgroups.TheinvitrostudyshowedthatCol1a1,Col3a1andαSMAexpressionsatbothmRNAandproteinlevelsweredown-regulatedbycarvedilolinratcardiacfibroblastsinadose-dependentmanner.Smad3inhibitors,SIS-3andnaringenin,couldefficientlydecreaseCol1a1,Col3a1andα-SMAexpressionsinratcardiacfibroblasts.Smad3wasshownsignificantlyinactivatedincarvedilol-treatedratcardiacfibroblasts.ConclusionCarvedilolnegativelyregulatesSmad3signalpathwayandinhibitsextracellularmatrixrelatedCol1a1,Col3a1andα-SMAexpressions,contributingtotheanti-fibrosiseffectofcarvedilolagainstAMI-inducedmyocardialfibrosisinrats.

简介：ObjectiveToobservetheeffectofaccessorypathway(AP)conductiononPJintervalinpatientswithWolff-Parkinson-Whitesyndrome.Methods129patientswithasinglemanifestationofAPwhounderwentsuccessfulradiofrequencyablation(RFCA)wereincluded.Patientsweredividedinto10groupsaccordingtoAPlocation.ThePRintervals,QRSdurationsandthePJintervalsweremeasuredusingsimultaneous12-leadECGbeforeandafterablation.ThePJintervalsbeforeablationwerecomparedwiththatafterablation.Theatrioventricular(AV)conductiontimeviaatrioventricularnode-HisconductionsystembeforeablationwerecomparedwiththePRintervalsafterablation.Theventriculardepolarizationtimeviaatrioventricularnode-HisconductionsystembeforeablationwerecomparedwiththeQRSdurationsafterablation.Deltawaveswerecomparedbetweeneachtwogroups.Results(1)ThePJintervalsofrightposterior(RP)groupandrightposteroseptal(RPS)groupbeforeablationwereshorterthanthatafterablation(RPgroup226±18msvs236±19ms,P<0.01,RPSgroup221±18msvs238±31ms,P<0.05,respectively).(2)Therewerenosignificantdifferencesbetweentheatrioventricular(AV)conductiontimeviaatrioventricularnode-HisconductionsystembeforeablationandthePRintervalsafterablation.(3)Theventriculardepolarizationtimeviaatrioventricularnode-HisconductionsystemofRPgroupandRPSgroupbeforeablationwereshorterthanthePRintervalsafterablation(RPgroup79±12msvs87±9ms,P=0.01;RPSgroup70±13msvs86±9ms,P<0.05,respectively).(4)ThedeltawavesofRPgroupandRPSgroupwerelongerthanthatofleftposteriorgroupandleftposteroseptalgroup(P<0.05).ConclusionPJintervalisshortenedbyAPconductionwhichpre-excitesthegenerallastexcitedpartofleftventricle.ItisdeterminedbyAPlocationandtheextentofpreexcitation.

简介：ObjectivesTounderstandtheeffectofcarvedilolonthecoronaryvascularendothelialfunctionofthepatientswithcoronaryheartdiseaseafterpercutaneoustransluminalcoronaryangioplasty(PTCA).Methods51cases,havingoneormorethantwobranchesnarrow(≥70%),werediagnosedbycoronaryangiography.Thesepatientsweredividedrandomlyintocarvedilolgroup(n=28)andcontrolgroup(n=23)whodidnottakecarvedilol.Endothelin(ET)andnitrodioxide(NO)levelsofperipheralbloodweremeasuredbeforeandafterPTCA,beforeandaftertwoweeksbytakingcarvedilol.ResuitsComparedwiththeETandNOlevelsbeforePTCA,ETweremarkedlyincreasedandNOweredecreasedafterPTCA(p<0.05);comparedwiththeETandNOlevelsbeforetakingcarvedilol,ETweredecreasedandNOwereincreasedaftertwoweek(p<0.05),buttheETandNOlevelsofthecontrolgroupdidnotchangeintheperiodoftwoweeksobservation(p>0.05).ConclusionsCarvedilolmayimprovethecoronaryvascularendothelialfunctionafterPTCA.

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：ObjectivesToinvestigatethechangesofβ3-adrenoceptor(β3-AR)mRNAexpressionintheratswithchronicheartfailure(CHF),andtoexploretheeffectofβblockers(βBs)onβ3mRNAexpression.MethodsThirty-fourratswererandomlydividedintoShamgroup(n=10)andheartfailuregroup(n=24).Ratmodelwasestablishedbyaorticconstriction.Thesurvivalratsinheartfailuregroupweredividedintoheartfailurecontrolgroup(HFgroup,n=6),metoprololgroup(METgroup,n=8)andcarvedilolgroup(CARgroup,n=8)threemonthsafteroperation.Metoprololtartartewasstartedorallywith12mg·kg-1·d-1,carvedilolwith6mg·kg-1·d-1,isometricsalinewasstartedinHFgroup.Afterthreemonthsofdrugtherapy,measurementofhemodynamics,indexofventricularmass,thelevelofβ3-ARmRNAexpressionwereperformed.ResultsComparedwithShamgroup,leftventricularendsystolicpressure(LVESP),andtheabsolutevaluesofmaximalrateofriseandfall(±dp/dtmax)ofleftventricularpressurewereallsignificantlydecreased(P<0.01),leftventricularenddiastolicpressure(LVEDP)wassignificantlyincreasedinHFgroup(P<0.01).ThehemodynamicparameterswereimprovedbyβBs,andcarvedilolwasmoreeffectivethanmetoprolol(P<0.01).TheindexofventricularmasswashigherinHFgroupthanMETgroup,CARgroupandShamgroup(P<0.01).βBssignificantlydecreasedtheindexofleftventricularmass(LVMI),andCarvedilolwasmoreeffectivethanmetoprolol(P<0.01).Theindexofrightventricularmass(RVMI)didnotchangeinMETgroup(P>0.05),butsignificantdecreasecouldbeseeninCARgroup(P<0.01).Thelevelofβ3-ARexpressioninleftventriclewasgreaterthanthatinrightventriclewhetherinthefailingheartorinthenon-failingheart.ComparedwithShamgroup,thelevelofβ3-ARmRNAexpressionwassignificantlyincreasedinHFgroup(P<0.01).Thelevelsofβ3-ARmRNAexpressionshowedaremarkabledecreaseinCARgroup(P<

简介：ObjectivesToevaluatetheeffectofdifferentstylesofcoronaryheartdisease(CHD),differentregionsofacutemyocardialinfarction(AMI),itsriskfactorsandbranchesofcoronarystenosisonleftventricularremodelinganddysfunctionbyapplyingechocardiography.Methods251patientswithCHDand96patientswithoutCHD(NoCHD)wereverifiedbyselectivecoronaryangiography.CHDpatientsweredividedintostableanginapectoris(SAP)26,unstableanginapectoris(UAP)53,acutemyocardialinfarction(AMI)140andoldmyocardialinfarction(OMI)30basedonclinicalsituation,cTnT,cardiacenzymeandEGG.AMIpatientswerefurtherdividedintosubgroupsincludingacuteanteriormyocardialinfarct(Aa,n=53),acuteinferiormyocardialinfarction(Ai,n,=54)andAa+Ai(n=33)basedonECG.Cardiacparameters:end-diastolicinterventricularseptumthickness(IVSd),end-diastolicleftventricularinternaldiameter(LVd),leftventricularmass(LM),end-diastolicleftventricularvolume(EDV),end-systolicleftventricularvolume(ESV)andleftventricularejectionfraction(LVEF)weremeasuredbyACUSON128XP/10echocardiography.MultipleslinearregressionanalyseswereperformedtoteststatisticalassociationsbetweenLVEFandtheinvolvedbranchesofcoronarystenosis,bloodpressure,lipids,glucoseandetcafteronsetofmyocardialinfarction.ResultsEDVandESVwereincreasedandLVEFdecreasedonpatientswithAMI,OMIandUAP(P<0.05-0.0001).LMwasmainlyincreasedinpatientswithOMI(P<0.01)andLVdwasmainlyenlargedinpatientswithAMI.EFwassignificantlydecreasedandEDV,ESV,LMandLVdwereremarkablyincreasedinAMIpatientswithAaandAa+Ai.WiththemultiplelinearregressionanalysesbySPSSsoftware,wefoundthatLVEFwasnegativelycorrelatedtotheinvolvedbranchesofcoronarystenosisaswellastosystolicbloodpressureafteronsetofmyocardialinfarctionwhiletherewasnosignificantcorrelationbetweenLVEFandotherfactors.LVEFwassignificantlydecreased,and

简介：ObjectivesTostudytheeffectoflatereperfusiononcaspase-3activityofischemicmyocardiuminrabbitanditssignificance.Methods24adultrabbitswererandomlydividedinto3groups:Sham(S)withoutligationofcoronaryartery,LateReperfusion(LR)withligationfor3hoursfollowingreleasefor3hoursandPersistentIschemia(PI)withpersistentligationofcoronaryarteryfor6hours.Allanimalsweresacrificed6hoursafterthebeginningoftheexperiments.BorderregionofinfarctedmyocardiumwereincisedforanalyzingtheconcentrationofSOD,MDA,GRandtheexpressionofFADD,Caspase-3andtheapoptosisindex(AI).ResultsComparedwiththeShamgroup,LRandPIgroupexhibitedmuchhigherMDA,FADD,Caspase-3,AIandmuchlowerSOD,GR(allP<0.01).ComparedwiththePIgroup,LRgroupexhibitedhigherMDA,FADD,Caspase-3,AIandlowerSOD,GR(allP<0.05).ConclusionsLatereperfusionmarkedlyenhancedtheCaspase-3activityandthenthenumberofapoptoticcardiomyocyteinborderregionofinfractedmyocardium,whichindicatedtheexistenceoflatereperfusioninjury.ThemechanismmayinvolvethehighoxidativestressstateandexpressionofFADD.

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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.