摘要
ObjectivesItisnotfullyclarifiedhowdiabetesmellitusinducedcardiacdysfunctionandmyocardialultrastructuralchangesintheearlystate.Inthepresentstudy,weprovidedanintegratedapproachtoinvestigateearlychangesinmyocardialfunctionofdiabeticrabbitsandassessedthestructuralalteration.MethodsandResultsDiabeteswasinducedbyalloxaninjection.After30days,echocardio-graphyandleftventricularcannulationwereperformedindia-betic(D,n=8)andcontrolrabbits(C,n=10).Aftercatheterization,animalswerekilledforhistologicalstudies.Hema-toxylin-eosinandMasson’sTrichromestainingoftheheartwereanalyzed.Theultrastructureofleftventriclewasalsoexaminedwithelectronmicroscopy.EchocardiographyrevealedthatearlydiabeticcardiomyopathyhadimpairedLVdiastolicfunctionexpressedbydiminishedE-waves,increasedAwaves,E/AratioreversionandincreasedE-wavedecelerationtime(EDT).Concurrently,LVend-diastolicpressure(LVEDP)anddiastolictimeconstant(T)wereincreased,minimumdP/dt(LV-dp/dt)wasreduced,obtainedthroughcardiaccatheterization.TherewerenosignificantdifferencesinLVejectionfraction(EF),LVpeaksystolicpressure(LVSP),ormaximumdP/dt(LV+dp/dt).Qualitativelightmicroscopyrevealednohistologicchangesinmyocardiumfromdiabeticrabbits.Themostevidentultrastructuralchangewasspottedmyofibrillardamage,whileinterstitialfibrosiswasslight.ConclusionsTheseresultssuggestthatearlydiabeticcardiomyopathyinanimalmodelischaracterizedbyleftventriculardiastolicdysfunction,bothimpairedactiverelaxationandincreasedpassivechamberstiffness.Whereas,leftventricularsystolicfunctioncanremainnormal.Itmightpartlycontributetomyofibrillardamage,butnotmyocardialfibrosis.
出版日期
2011年01月15日（中国期刊网平台首次上网日期，不代表论文的发表时间）
