摘要
Insufficientgrowthandrarefactionofcapillaries,followedbyendothelialdysfunctionmayrepresentoneofthemostcriticalmechanismsinvolvedinheartdamage.Inthisstudyweexaminedhistochemicalandultrastructuralchangesinmyocardialcapillaryendotheliumintwomodelsofheartfailurestreptozotocin-induceddiabetesmellitus(STZ)andNOdeficienthypertensioninmaleWistarrats.Diabeteswasinducedbyasinglei.v.doseofSTZ(45mg/kg)andchronic9-weekstagewasanalysed.ToinduceNO-deficienthypertension,animalsweretreatedwithinhibitorofNOsynthaseLnitroargininemethylester(L-NAME)(40mg/kg)for4weeks.Leftventriculartissuewasprocessedforenzymecatalytichistochemistryofcapillaryalkalinephosphatase(AlPh),dipeptidylpeptidaseⅣ(DPPⅣ),andendothelialNOsynthase/NADPH-diaphorase(NOS)andforultrastructuralanalysis.Indiabeticandhypertensiverats,lower/absentAlPhandDPPⅣactivitieswerefoundinfocalmicro-areas.NOSactivitywassignificantlyreducedandpersistedonlylocally.QuantitativeevaluationdemonstratedreductionofreactionproductintensityofAlPh,DPPandNOSby49.50%,74.36%,20.05%indiabeticand62.93%,82.71%,37.65%inhypertensiverats.Subcellularalterationsofendothelialcellswerefoundinheartofbothgroupssuggestinginjuryofcapillaryfunctionaswellascompensatoryprocesses.Endothelialinjurywasmoresignificantindiabeticanimals,incontrasttheadaptationwasmoreevidentinhypertensiveones.Concluding:bothSTZ-induceddiabetes-andNO-deficienthypertension-relatedcardiomyopathywereaccompaniedbysimilarfeaturesofstructuralremodellingofcardiaccapillarynetworkmanifestedasangiogenesisandangiopathy.Thelatterwashowever,predominantandmayacceleratedisappearanceofcapillaryendotheliumcontributingtomyocardialdysfunction.
出版日期
2005年07月17日（中国期刊网平台首次上网日期，不代表论文的发表时间）
