[Membrane-protective effect of finoptin in exertion-induced stenocardia]

Ninety five males of employable age who suffered from effort-associated angina were examined. As the severity of angina increased, the structural disorganization of the lipid bilayer progressed in the erythrocyte membranes, resulting in abnormal functional status of Na+,K+- and Ca2+-ATPases and in accumulation of Ca2+ and Na in the intracellular space, by lowering potassium levels. Finoptin given to patients with angina not only diminished intracellular calcium concentrations, but produced membrane-protective effects by lowering malonic dialdehyde levels in the lipid bilayer of the cellular membranes, by accumulating phospholipids and cholesterol esters, and returning the values of Na+,K+- and Ca2+-ATPase activities to controls. A parallelism was found between the magnitude of the membrane-protective action of finoptin in patients with angina and its antianginal effect.