Kokarev A N, Kardakov Iu I
Kardiologiia. 1989 Jul;29(7):21-5.
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.
对95名处于就业年龄且患有劳力性心绞痛的男性进行了检查。随着心绞痛严重程度的增加，红细胞膜脂质双层的结构紊乱加剧，导致Na⁺、K⁺ - 和Ca²⁺ - ATP酶的功能状态异常，细胞内空间中Ca²⁺和Na积累，同时钾水平降低。给予心绞痛患者的芬普替林不仅降低了细胞内钙浓度，还通过降低细胞膜脂质双层中的丙二醛水平、积累磷脂和胆固醇酯以及使Na⁺、K⁺ - 和Ca²⁺ - ATP酶活性值恢复到对照水平，产生了膜保护作用。在心绞痛患者中，发现芬普替林的膜保护作用大小与其抗心绞痛作用之间存在平行关系。
