大鼠心肌整体缺血及离体再灌注致生物膜的损伤作用

目的和方法：利用整体大鼠异丙肾上腺素损伤（ISO）和离体大鼠全心停灌／再灌（I／R）两种模型,观察了心肌缺血和缺血／再灌注对心肌生物膜－线粒体膜及肌纤维膜损伤的影响。结果：ISO（5mg/kg,皮下注射）和I／R（20min/20min)可导致大鼠心脏生物膜产生严重损伤,表现为心肌线粒体脂质过氧化产物明显增加,线粒体磷脂酶A2（PLA2）激活,从而导致线粒体膜磷脂（PL）含量减少,磷脂分解产物游离脂肪酸（FFA）增加,膜脂流动性（LFU）降低,线粒体Ca^2 -ATPase及肌纤维膜Na^ ,K^ -ATPase活性降低,线粒体呼吸功能降低、呼吸链氧化磷酸化解偶联,高能磷酸化合物生成减少。结论：整体ISO和离体I／R可导致大鼠心肌线粒体、肌纤维膜结构和功能损伤。

Biomembrane damages induced by in vivo and in vitro myocardial ischemia and reperfusion in rats

Aim and Methods: Using in vivo myocardial injury model induced by Isoproterenol (ISO) and the model induced by in vitro global heart ischemia/reperfusion (I/R) in rats,we observed the effects of myocardial ischemia and ischemia/reperfusion on bio-membranes of mitochondria and sarcolemma injury. Results: ISO (5 mg/kg,s.c.) and I/R (20 min/20 min) damaged myocardial bio-membranes of rat,in which the lipid peroxidation of mitochondria was significantly increased,the activity of phospholipase A 2 was activated and the contents of phospholipid and free fat acid were decreased and increased significantly,respectively. The membrane lipid fluidity and the activities of Ca 2+-ATPase of mitochondria and Na +,K +-ATPase of sarcolemma were significantly lowered. In addition,the respiration function of mitochondria was declined and the oxidative phosphorylation of respiratory chain was uncoupled,which resulted in the decrease in the production of high energy phosphoric acid compounds. Conclusion: Myocardial injuries caused by ISO or I/R injured the structure and function of rat myocardial mitochondria and sarcolemma.