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磷脂酶A_2(EC3.1.1.4,PLA_2)及其水解产物在心肌梗塞及缺血方面的研究已有十几年的历史,现已证明PLA_2广泛存在于机体的各种细胞中,参与细胞及细胞内膜的代谢。心梗时由于心肌缺血,导致该酶的活性增强,并水解心肌细胞膜上的磷脂转化成具有毒性的脂肪酸和溶血磷脂(主要为溶血卵磷脂),故加速了心肌的坏死,而被称之为有害酶。心梗后血清PLA_2的升高水平与心肌坏死的范围、大小呈正相关,因而在心梗的应用上血清PLA_2比传统的“心肌酶”及心电图更有价值。动物试验表明:使用特异性PLA_2抑制治疗心梗,可有效的降低PLA_2活性,使心肌坏死的面积减少50%以上。本文
Phospholipase A2 (EC3.1.1.4, PLA2) and its hydrolyzate in myocardial infarction and ischemia has been more than 10 years of history, PLA2 has been widely found in a variety of cells in the body, involved in cells and Cell membrane metabolism. Myocardial infarction due to myocardial ischemia, resulting in enhanced activity of the enzyme, and the hydrolysis of myocardial cell membrane phospholipids into toxic fatty acids and lysophosphatides (mainly lysophosphatidylcholine), it accelerated myocardial necrosis, which is called For harmful enzymes. The level of serum PLA_2 after myocardial infarction is positively correlated with the range and size of myocardial necrosis, and therefore serum PLA_2 is more valuable than traditional “myocardial enzymes” and electrocardiogram in myocardial infarction. Animal experiments show that: the use of specific inhibition of PLA2 treatment of myocardial infarction, PLA2 activity can be effectively reduced, so that the area of myocardial necrosis reduced by 50%. This article