Kuzuya T, Fuji H, Hoshida S, Kitabatake A, Tada M
First Department of Medicine, Osaka University School of Medicine, Japan.
Jpn Circ J. 1991 Nov;55(11):1127-31. doi: 10.1253/jcj.55.1127.
Free radicals derived from polymorphonuclear leukocytes (PMN) have been suggested to play an important role in myocardial ischemia-reperfusion injury. To define the mechanism by which activated PMN exacerbate ischemic myocardial damage, we investigated the extent of cell injury, free radical generation and lipid peroxidation in embryo mouse myocardial cells co-incubated with activated PMN. The generation of free radicals derived from PMN correlated with the extent of myocardial cell injury. Among the cell sheets preconditioned with hypoxic and glucose free medium, PMN-adhered myocardial cells were initially injured after adding PMN activator, extending to adjacent cells. Chemiluminescence emission and thiobarbituric acid reactive substance in the co-incubated cells were markedly increased and sustained compared with those in each cell monoincubation. The augmented lipid peroxidation was related to the progression of myocardial cell injury. These results indicate that PMN-derived free radicals cause membrane disruption, contributing to the progression of myocardial injury.
多形核白细胞（PMN）衍生的自由基被认为在心肌缺血再灌注损伤中起重要作用。为了确定活化的PMN加重缺血性心肌损伤的机制，我们研究了与活化的PMN共同孵育的胚胎小鼠心肌细胞中的细胞损伤程度、自由基生成和脂质过氧化情况。PMN衍生的自由基生成与心肌细胞损伤程度相关。在经缺氧和无糖培养基预处理的细胞片中，添加PMN激活剂后，黏附PMN的心肌细胞最初受到损伤，并扩展至相邻细胞。与各细胞单独孵育相比，共同孵育细胞中的化学发光发射和硫代巴比妥酸反应性物质显著增加且持续存在。脂质过氧化增加与心肌细胞损伤的进展有关。这些结果表明，PMN衍生的自由基导致膜破坏，促进心肌损伤的进展。
