简介：ObjectivesToinvestigateeffectofAngll,captoprilonsingleguineamyocytesonL-typecalciumcurrentandsodiumcurrent.MethodsMembranepatchclampwholecellrecordingtechniquewasusedtoinvestigateeffectofangll,captoprilonL-Camaximumcurrentdensityandsodiummaximumcurrentdensity.ResutlsAngllincreasedthemaximumcurrentdensitycomparedwithcontrolafterperfused5min,357.7±219.7Vs279.5±240.5PA/PF,increaserateis27.9%,theshapeofcurrent-voltagerelationshipcurvewasunchanged,peakedat+10mv,indicatedthatangllincreasedL-Cacurrentdensityinvoltage-dependent.Afterperfusedwithcaptopril,captopril+angll3,5min,L-Cacurrentwasrecorded,resultssuggestL-Camaximumcurrentdensitydecreasedsignificantlycomparedwithcontrol,incaptoprilgroup,128.4±92.6Vs286.2±89.7,66.7±68.3Vs286.2±89.7,respectively,rateofinhibitionis55.1%,76.6%,respectively.L-Cacurrentfurtherdecreasedincaptoprilpe

简介：BackgroundTreatmentofratswiththebeta-adrenergicagonistIsoprenaline(ISO)resultsincardiachypertrophyandmyocardialfibrosis.Inthepresentwork,weaimedtostudytheinvivoeffectsofISOonserumlevelsofmonocytechemoattractantprotein-1andtissueinhibitorofmatrixmetalloproteinasestypeIinWistarrats.MethodsISO(5mg·kg-1)orSalinewereinjectedsubcutaneouslyintoWistarratsonceadayfor3or7consecutivedays.Ventricularremodelingandcardiacfunctionwereevaluatedbyechocardiography.Sectionsofheartwerestainedwithhematoxylin-eosin(HE)forhistopathologyorwithMassonstrichromeforcollagenvisualization.Inaddition,hearttissueimmunohistochemistryforɑ-SMAwasalsoanalyzed.TheserumlevelsoftissueinhibitorofmatrixmetalloproteinasestypeI(TIMP-1)andmonocytechemoattractantprotein-1(MCP-1)weredeterminedbyLuminexmultiplextechnology.ResultsISOinducedcardiacdysfunctioninratsafter3or7daysoftreatment.ISOcausedsignificantincreaseofmyocardialdisorderandfibrosiswithincreasedɑ-SMAexpression.ISOtreatedaatsshowedasignificantincreaseintheserumlevelsofTIMP-1andMCP-1.ConclusionsOurstudysuggeststhatISOinducesprofoundcardiacremodelingaccompaniedwithincreaseofserumTIMP-1andMCP-1.