Borinskiĭ Iu N, Paramonova I V, Kornyshev S N
Vopr Med Khim. 1993 Nov-Dec;39(6):20-2.
Lipid composition was studied in various zones of the myocardium impaired with infarction. Content of phospholipids was decreased, while lysophospholipids and free fatty acids were increased in the necrosis-impaired sites. In the overinfarction-impaired tissues content of total lipids, triglycerides, cholesterol and its esters and free fatty acids was elevated but some phospholipids were decreased (cardiolipins, phosphatidyl ethanolamine and sphingomyelins). Alterations in lipid composition observed in necrosis impaired myocardial tissues appear to occur due to destruction of cardiomyocytes, to the following liberation of enzymes from the cells and their irregular effects on lipid metabolism. There were apparently three types of reactions in the overinfarction-impaired sites: hydrolysis of lipids, decrease in the rate of fatty acids oxidation and increase--in synthesis of individual lipid classes. All the alterations detected were related to deficiency in oxygen, accumulation of NADH2, NADPH2 and factate. This suggests that activation of biosynthesis of free fatty acids and lipids, directed to neutralization of the dehydrogenase coenzymes and to continuation of glycolysis, may be involved in positive compensation-adaptive reactions during definite steps of the disease development. However, during the further steps of the disease increase in content of free fatty acids and other lipids in blood and tissues, as in the case of lactate, may aggravate the pathological state, acquired dysfunction and increased the necrosis-impaired zone. The data obtained suggest that analysis of lipid spectrum in various myocardial tissues may exhibit the rate of hypoxic and ischemic alterations, demonstrated the reserves of metabolic activity as well as showed the risk of necrosis enlargement during the prelethal period of the disease.
对梗死受损心肌的不同区域的脂质成分进行了研究。在坏死受损部位,磷脂含量降低,而溶血磷脂和游离脂肪酸含量增加。在梗死灶周围受损组织中,总脂质、甘油三酯、胆固醇及其酯类和游离脂肪酸含量升高,但一些磷脂(心磷脂、磷脂酰乙醇胺和鞘磷脂)含量降低。坏死受损心肌组织中观察到的脂质成分变化似乎是由于心肌细胞的破坏,随后细胞内酶的释放及其对脂质代谢的不规则影响所致。在梗死灶周围受损部位显然存在三种反应类型:脂质水解、脂肪酸氧化速率降低以及个别脂质类别的合成增加。检测到的所有变化都与缺氧、NADH2、NADPH2和乳酸的积累有关。这表明,游离脂肪酸和脂质生物合成的激活,旨在中和脱氢酶辅酶并维持糖酵解,可能参与了疾病发展特定阶段的正向代偿适应性反应。然而,在疾病的进一步发展阶段,血液和组织中游离脂肪酸和其他脂质含量的增加,就像乳酸的情况一样,可能会加重病理状态、获得性功能障碍并扩大坏死受损区域。所获得的数据表明,分析不同心肌组织中的脂质谱可能显示缺氧和缺血改变的速率,展示代谢活动的储备,并显示疾病致死前期坏死扩大的风险。