[The role of structural changes of the endothelium and myocardium in the development of experimental heart failure].

The aim of the investigation was to study the role of structural myocardial and endothelial reorganization during the experimental heart failure (doxorubicin model). Rat endocardial and aortal endothelium as well as left ventricular myocardium, were studied using the methods of light and electron microscopy and immunocytochemistry (TUNEL-assay). The major regularities of structural and functional myocardial and endothelial reorganization were determined in rats with an experimental heart failure. The pronounced cardiomyocyte (CMC) heteromorphism was found. CMCs with the signs of hypertrophy and hyperplasia were identified together with the CMCs showing discomplexation of sarcomeres and fragmentation of myofibrils, CMCs with the numerous caveolae, liposomes, autophagosomes and myelin-like bodies. The peculiarities of the ultrastructural changes were established in the endocardial and aortal endothelium. The increase in CMC and endothelial cell number showing the signs of apoptosis, was demonstrated. The role of structural and functional myocardial and endothelial reorganization during experimental heart failure is discussed.

[Effects of endotheline and nitric oxide on vascular tonicity in patients with chronic cardiac failure].

AIM: To examine effects of endotheline-1 (ET-1) and nitric oxide (NO) on endothelium-dependent mechanisms of vascular tonicity regulation in patients with chronic cardiac failure (CCF) of FC I-IV (NYHA). MATERIAL AND METHODS: Vascular reactions of 94 patients with CCF of FC I-IV were examined according to D.S. Celermajer method using ultrasound of high resolution. Tissue oxygenation was studied with transcutaneous polarography (TCM-2, Radiometer). Parameters of circulating erythrocytes were studied by impurity spectrum. Endothelial NO-synthase expression was determined with application of monoclonal antibodies to endothelial NO-synthase. NO metabolites were studied with colorimetric method using Griss reagent. ET-1 was measured in plasma by enzyme immunoassay. The control group consisted of 28 healthy men aged 20 to 54 years. RESULTS: Patients with CCF of FC I-IV have reduced endothelium-dependent vascular reactions progressing with aggravation of CCF. The causes of the disorders lie in altered metabolism of ET-1 and NO in CCF. CONCLUSION: CCF patients demonstrate changes in endothelium-dependent mechanisms of vascular tonicity regulation caused by disturbed metabolism of ET-1 and NO developing in abnormal regime of tissue oxygenation and depending on CCF severity.