[Structural and metabolic aspects of heterogenicity of the ventricular cardiac myocytes in coronary insufficiency].

The paper shows comparative analysis of structural-metabolic changes of the ventricular cardiac hystiocytes during transitional restriction of blood supply, which leads to relapsing myocardium hypoperfusion, ischemia and even to cardiac infarction. We have established that an increase of the myocardium arrhythmogenicity, damage of myocardium electrophysiological activity and coronary deficiency are caused by pathologically intensified structural-metabolic heterogeneity of cardiomyocites. The chronic ischemic heart disease is worsening the situation by gradual accumulation of the metastructure changes of heart's working cells.

[Effect of long term administration of finoptin on the morphofunctional state of working cells of the intact myocardium in modeling of chronic coronary insufficiency].

In accordance with the findings on the key role of the cardiomyocite electrolyte homeostasis abnormality in dysfunction and coronary insufficiency-related alterative changes in the contractile myocardium and positive results of correction of the above abnormalities with Ca2+ antagonists morphofunctional aspects were studied of cardioprotective action of finoptin in its course administration in experiments in rabbits. General histological techniques were used together with transmission electron microscopy and cytochemical tests. The drug under study has been shown to increase the cardiomyocite glyco-calyx Ca(2+)-depositing function and to diminish its quickly-exchanging fraction on a plasmolemma.

[Morphofunctional aspects of cardioprotective effect of propranolol in modelling of chronic ischemic heart disease].

In experiments involving simulation of ischemic heart disease in adult rabbits, morphofunctional aspects were studied of cardioprotective action of propranolol on the contractile myocardium. With the aid of histological and histochemical, electron microscopic tests, the drug under consideration has been shown to be endowed with membrane-stabilizing properties, quite aside its receptor-mediated effects on Ca2+ metabolism known for. A decrease in its excessive ingress into the sarcoplasma comes, in its turn, to improve energy and plastic maintenance of the myocardial functions, to moderate a pathological reorganization and destructive changes in cardiomyocytes, thus promoting the contractile myocardium resistance to recurrent coronary crises.