[Cellular beta-adrenergic receptor complex in patients with heart failure and its changes during digoxin therapy].

Twenty eight males with dilated cardiomyopathy, 5 males with coronary heart disease concurrent with postinfarction cardiosclerosis, 4 males and 2 females with rheumatic heart disease were examined. The findings suggest desensitization of the cellular beta-adrenoreceptor complex in patients with circulatory failure, which appeared as lower beta-adrenoreceptor density with cardiac decompensation progression and impaired transmission of a hormonal signal in the cell, particularly in patients with dilated cardiomyopathy. Digoxin therapy let to an increase in beta-adrenoreceptor density with its initial decrease and to adenylate cyclase activity enhancement. The absence of a positive ++clinico-hemodynamic effect and time course of plasma catecholamine levels in some patients with severe circulatory failure during digoxin use, as well as no changes in the values of the beta-adrenoreceptor adenylate cyclase complex indicate that the abnormalities in beta-adrenergic regulation play an important role in the pathogenesis of refractoriness at the cellular level. Retention of forskolin's stimulant effect allows one to expect a significant positive therapeutic response to be shown with the usage of drugs whose load point is a catalytic subunit of adenylate cyclase.