Zarubina E G
Voen Med Zh. 2002 Feb;323(2):34-6, 96.
The patients with myocardial infarction have marked changes in the structure of both protein and lipid parts of the membrane. These changes are connected with destruction of antioxide cell protection against the background of developing hypoxia and "oxide stress". In such patients the increase in HbA2 and HbF factors may be regarded as the adaptive mechanism of hypoxia conditions that develop due to decrease in myocardial propulsive ability and deterioration of blood rheological properties. Change of structural and functional characteristics of erythrocyte membranes leads to increase in their hardness that is connected with the increase in blood viscosity, pressure upon the impaired myocardium and extension of necrotic zones. Similar structures of erythrocyte and cardiomyocyte membranes allow to draw a conclusion about the presence of similar disorders in the latter membranes. It shows the necessity to introduce into the treatment scheme of myocardial infarction patients the drugs inhibiting lipid oxidation.
心肌梗死患者的细胞膜蛋白质和脂质部分结构均有显著变化。这些变化与在缺氧和“氧化应激”发展背景下抗氧化细胞保护作用的破坏有关。在这类患者中，HbA2和HbF因子的增加可被视为由于心肌推进能力下降和血液流变学性质恶化而产生的缺氧状态的适应性机制。红细胞膜结构和功能特性的改变导致其硬度增加，这与血液粘度增加、受损心肌上的压力以及坏死区域的扩大有关。红细胞膜和心肌细胞膜的相似结构使得可以得出结论，后者的膜中存在类似的紊乱。这表明有必要在心肌梗死患者的治疗方案中引入抑制脂质氧化的药物。
