心肌线粒体ATP敏感性钾通道开放保护线粒体结构和功能

目的　评价线粒体ATP敏感性钾通道 (mitoKATP)开放剂二氮嗪对缺氧心肌线粒体结构和功能的影响。方法　异丙肾上腺素 (ISO)皮下注射诱发大鼠心肌缺氧损伤 ,观察二氮嗪对线粒体呼吸控制比 (RCR)、膜流动性、磷脂酶A2 和磷脂含量的影响。结果　ISO皮下注射诱发大鼠心肌缺氧损伤后 ,与对照组比较线粒体RCR降低了 2 0 8% (P <0 0 1) ,膜流动性降低了 9 1% (P <0 0 5 ) ,磷脂酶A2 活性增加了14 4 5 % (P <0 0 1) ,磷脂含量下降了 37 5 % (P <0 0 5 ) ,二氮嗪预防性给药后可改善RCR、膜流动性和磷脂含量。结论　二氮嗪可保护心肌缺氧损伤后线粒体膜结构和功能的完整

Effects of mitochondrial ATP-sensitive potassium channel opener on the structures and functions of the mitochondria

AIM To evaluate the effects of diazoxide on the structures and functions of the mitochondria after hypoxia injury. METHODS A myocardial hypoxia injury model on rat is established by subcutaneous injection of isoproterenol (ISO) 5 mg·kg -1. The degree of oxidative phosphorylation, membrane lipid fluidity (LFU), phospholipidase A 2 activity, and phosphlipid content of mitochondria were observed after hypoxia injury. RESULTS Compared with the controls, the levels of RCR, LFU and phosphlipid content were decreased 20.8% (P<0.01), 9.1% and 37.5% (P<0.05), respectively. PLA 2 were increased by 144.5%(P<0.01). Administration of diazoxide increased RCR, LFU and phosphlipid content. CONCLUSION These results suggest that diazoxide has a protective effect on ISO-induced myocardial injury in rats.