[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.
Kokarev
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Kardakov
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D000328:Adult; D000787:Angina Pectoris / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D002118:Calcium / Q000037:antagonists & inhibitors / Q000097:blood*; D000252:Calcium-Transporting ATPases / Q000097:blood; D004910:Erythrocyte Membrane / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D005082:Physical Exertion; D011188:Potassium / Q000037:antagonists & inhibitors / Q000097:blood*; D012964:Sodium / Q000037:antagonists & inhibitors / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood; D014700:Verapamil / Q000627:therapeutic use*
D012964:Sodium; D014700:Verapamil; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium
Membranoprotektornyĭ éffekt finoptina pri stenokardii napriazheniia.