Kawaguchi H, Yasuda H
Department of Cardiovascular Medicine, Hokkaido University, School of Medicine, Sapporo, Japan.
Circ Res. 1988 Jun;62(6):1175-81. doi: 10.1161/01.res.62.6.1175.
Phospholipid metabolism was studied in rat myocardial slices that were incubated under normoxia or hypoxia for up to 24 hours. Phospholipid degradation was prominent in hypoxic myocardium, particularly phosphatidylcholine, which markedly decreased after 24 hours of hypoxia. In contrast, lysophosphatidylcholine increased. The mechanism of phospholipid degradation in hypoxic myocardium was studied. The highest activity for phospholipase A2 among subcellular fractions was found in microsomal fraction. In hypoxic myocardium, this phospholipase A2 activity markedly increased and had substrate specificity toward phosphatidylcholine and phosphatidylethanolamine. Phosphatidylcholine was slightly hydrolyzed in control myocardium, but it was markedly hydrolyzed in hypoxic myocardium. Phospholipase C activity was found in cytosol and had a high substrate specificity toward phosphatidylinositol. In hypoxic myocardium, its activity gradually decreased during hypoxic incubation. Prostacyclin biosynthesis was also determined. The synthesis of prostacyclin in hypoxic myocardial microsomes did not increase. These results suggest that hypoxia causes phospholipid degradation and activates phospholipase A2 activity.
在常氧或缺氧条件下孵育长达24小时的大鼠心肌切片中研究了磷脂代谢。磷脂降解在缺氧心肌中很明显，尤其是磷脂酰胆碱，在缺氧24小时后显著减少。相比之下，溶血磷脂酰胆碱增加。研究了缺氧心肌中磷脂降解的机制。在亚细胞组分中，磷脂酶A2的活性最高的是微粒体组分。在缺氧心肌中，这种磷脂酶A2的活性显著增加，并且对磷脂酰胆碱和磷脂酰乙醇胺具有底物特异性。在对照心肌中磷脂酰胆碱略有水解，但在缺氧心肌中它被显著水解。磷脂酶C的活性存在于胞质溶胶中，并且对磷脂酰肌醇具有高底物特异性。在缺氧心肌中，其活性在缺氧孵育期间逐渐降低。还测定了前列环素的生物合成。缺氧心肌微粒体中前列环素的合成没有增加。这些结果表明，缺氧导致磷脂降解并激活磷脂酶A2的活性。
