论文部分内容阅读
Insufficient growth and rarefaction of capillaries, followed by endothelial dysfunction may represent one of the mostcritical mechanisms involved in heart damage. In this study we examined histochemical and ultrastructural changes inmyocardial capillary endothelium in two models of heart failure streptozotocin-induced diabetes mellitus (STZ) and NO-deficient hypertension in male Wistar rats. Diabetes was induced by a single i.v. dose of STZ (45 mg/kg) and chronic 9-week stage was analysed. To induce NO-deficient hypertension, animals were treated with inhibitor of NO synthase L-nitroarginine methylester (L-NAME) (40 mg/kg) for 4 weeks. Left ventricular tissue was processed for enzyme cata-lytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NOsynthase/NADPH-diaphorase (NOS) and for ultrastructural analysis. In diabetic and hypertensive rats, lower/absentAlPh and DPP IV activities were found in focal micro-areas. NOS activity was significantly reduced and persisted onlylocally. Quantitative evaluation demonstrated reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%,74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. Subcellular alterations of endothelialcells were found in heart of both groups suggesting injury of capillary function as well as compensatory processes.Endothelial injury was more significant in diabetic animals, in contrast the adaptation was more evident in hypertensiveones. Concluding: both STZ-induced diabetes- and NO-deficient hypertension-related cardiomyopathy were accompa-nied by similar features of structural remodelling of cardiac capillary network manifested as angiogenesis and angiopathy.The latter was however, predominant and may accelerate disappearance of capillary endothelium contributing to myo-cardial dysfunction.
Insufficient growth and rarefaction of capillaries, followed by endothelial dysfunction may represent one of the most critical mechanisms involved in heart damage. In this study we observed histochemical and ultrastructural changes in myocardial infarction in two models of heart failure streptozotocin-induced diabetes mellitus (STZ) and NO-deficient hypertension in male Wistar rats. Diabetes was induced by a single iv dose of STZ (45 mg / kg) and chronic 9-week stage was analysed. To induce NO-deficient hypertension, animals were treated with inhibitor of NO synthase L Left ventricular tissue was processed for enzyme cata-lytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NO synthase / NADPH (L-NAME) -diaphorase (NOS) and for ultrastructural analysis. In diabetic and hypertensive rats, lower / absent AlPh and DPP IV activities were found in focal micro-areas. NOS activity w Aspect reduced evaluation and reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%, 74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. Subcellular alterations of endothelial cells found in heart of both groups suggesting injury of capillary function as well as compensatory processes. Endothelial injury was more significant in diabetic animals, in contrast the adaptation was more evident in hypertensiveones. Concluding: both STZ-induced diabetes- and NO-deficient hypertension- related cardiomyopathy were accompa-nied by similar features of structural remodeling of cardiac capillary network manifested as angiogenesis and angiopathy. latter latter, predominant and may accelerate disappearance of capillary endothelium contributing to myo-cardial dysfunction.