【摘要】 目的观察线粒体内膜三磷酸腺苷敏感钾离子通道开放剂二氮嗪加入停搏液内对缺血再灌注大鼠心肌能量代谢的保护作用。方法50只大鼠随机分为五组,每组10只,取离体心脏;A组取正常心肌,其余制备离体工作心脏灌注模型;B组停灌30min,复灌60min;其余三组分别灌注不同的停搏液,C组灌注停搏液,D组灌注含二氮嗪的停搏液,E组灌注含二氮嗪停搏液之前10min给予格列苯脲,各组复灌30min后进行工作模式心脏灌注,监测心率、左室收缩峰压和舒张末压。实验终了取心肌,提取线粒体,测定细胞色素氧化酶活性、线粒体H+-三磷酸腺苷酶活性;高效液相法测定心肌含量。结果缺血再灌注心肌线粒体细胞色素氧化酶活性和线粒体H+-三磷酸腺苷酶活性降低(P<0.05);而二氮嗪处理组相应指标显著改善(P<0.01)。结论含二氮嗪停搏液能够改善缺血再灌注心肌功能,能量代谢恢复。更多还原

【Abstract】 Objective To evaluate the effects of mitochondrial ATP-sensitive potassium channel opener diazoxide on energy metabolism during ischemic and reperfusion in rats. Methods Fifty rats were divided into 5 groups randomly. Isolated working rat heart model was established. Control group(B) underwent 30-minute ischemia and 30-minute reperfusion. Group C and D were treated with st. Thomas Ⅱ cardioplegia and Diazoxide+st. Thomas Ⅱ cardioplegia before ischemia respectively. And group E was treated with glibenclamide 10min before giving Diazoxide+st. Thomas Ⅱ cardioplegia. In the end, HP, LVPSP and LVEDP were evaluated; and COX, H+-ATT and ATP were evaluated too. Results Compared with the controls, the levels of COX, H+-ATP, ATP and heart function were significantly increased(P<0.01). In group D, the heart was protected effectively by treatment of Diazoxide. Conclusion These results suggest that diazoxide has a cardioprotective effect on energy metabolism during ischemic and reperfusion in rat.更多还原