Role of phospholipases A2 and C in myocardial ischemic reperfusion injury.
Role of phospholipases A2 and C in myocardial ischemic reperfusion injury.
复制标题
磷脂酶 A2 和 C 在心肌缺血再灌注损伤中的作用。
DOI：
10.1152/ajpheart.1991.260.3.h877
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Das,DK
中科院分区：
文献类型：
--
作者：
Prasad,MR;Popescu,LM;Moraru,II;Liu,XK;Maity,S;Engelman,RM;Das,DK
本实验观察了磷脂酶A2（PLA2）和磷脂酶C（PLC）在缺血再灌注心肌磷脂降解和细胞损伤中的作用。为此，离体大鼠心脏灌注同位素花生四烯酸标记其膜磷脂。与非免疫球蛋白G预灌注的心脏相比，在常温下全脑缺血30分钟后再灌注30分钟，用抗磷脂酶A2（抗PLA2）预灌注的心脏保留了显著较高量的磷脂酰胆碱和磷脂酰肌醇的放射性标记，而溶血磷脂酰胆碱和非酯化脂肪酸的放射性标记量相应较低（P <0.05）。在类似的实验中，与非免疫球蛋白G处理的心脏相比，抗磷脂酶C（抗PLC）处理的心脏与所有磷脂中显著（P <0.05）较高的放射性标记和较低的放射性标记相关。这些心脏的亚细胞器中的磷脂酶活性的测量显示，抗PLA2处理的心脏的胞质溶胶，线粒体和微粒体中的PLA2活性降低，抗PLC处理的心脏的微粒体中的PLC活性降低。此外，这两种抗磷脂酶减弱肌酸激酶和乳酸脱氢酶释放到灌注液和增加收缩力，以及冠状动脉流量在再灌注心脏。本研究的结果表明，磷脂酶A2和PLC参与的磷脂降解和细胞损伤，发生在缺血心肌再灌注。
We investigated the role of phospholipase A2 (PLA2) and phospholipase C (PLC) in myocardial phosholipid degradation and cellular injury during reperfusion of ischemic myocardium. For this purpose, isolated rat hearts were perfused with isotopic arachidonic acid to label its membrane phospholipids. Hearts preperfused with antiphospholipase A2 (anti-PLA2) retained a significantly higher amount of radiolabel in phosphatidylcholine and phosphatidylinositol and a corresponding lower amount of radiolabel in lysophosphatidylcholine and nonesterified fatty acids (P less than 0.05) after 30 min of reperfusion following 30 min of normothermic global ischemia compared with hearts preperfused with nonimmune immunoglobulin G. In similar experiments, antiphospholipase C (anti-PLC)-treated hearts were associated with significantly (P less than 0.05) higher radiolabel in all phospholipids and lower radiolabel in diacyglycerol compared with nonimmune immunoglobulin G-treated hearts. Measurement of phospholipase activity in subcellular organelles of these hearts showed decreased PLA2 activity in cytosol, mitochondria, and microsomes of anti-PLA2-treated hearts and decreased PLC activity of microsomes in anti-PLC-treated hearts. Furthermore, both the antiphospholipases attenuated the release of creatine kinase and lactate dehydrogenase into perfusate and increased contractility as well as coronary flow in the reperfused hearts. Results of this study suggest that both PLA2 and PLC are involved in the degradation of phospholipids and cellular injury that occur during reperfusion of ischemic myocardium.