摘要
目的 观察异丙酚预处理对心肌缺血再灌注损伤的保护机制是否通过开放线粒体ATP敏感性K通道 (KATP)。方法 非循环式Langendorff离体心脏灌注模型 ,灌注 1h ,常温下行全心缺血 2 5min ,恢复再灌注 30min。通过Maclab仪记录左室舒张末压 (LVEDP)、左室发展压 (LVDP)、左室压上升和下降最大速率 (±dp/dtmax)。测恢复再灌注末心肌组织MDA含量。结果 恢复再灌注 30min末 ,对照组(Con)、异丙酚预处理组 (PP)、5 HD +PP和 5 HD组心肌组织的MDA含量分别为 (113 7± 2 0 9)、(89 4± 13 7)、(91 9± 14 4 )和 (114 8± 19 7)nmol·10 0mg-1。PP组和 5 HD+PP组的心肌MDA含量都明显低于Con组和 5 HD组 (P<0 0 5 ) ;PP组和 5 HD +PP组两组间的MDA差异无显著性 (P >0 0 5 )。恢复再灌注 30min末 ,Con组、PP组、5 HD+PP组和 5 HD组的LVEDP值分别为基础值的 5 1、3 2、3 6和 5 3倍。PP组和 5 HD +PP组LVEDP值的上升幅度均明显低于Con组和 5 HD组 (P <0 0 5 ) ,而 5 HD +PP组和PP组之间差异无显著性 (P >0 0 5 )。结论 异丙酚预处理的心肌保护不是通过开放线粒体ATP敏感性K通道 。
AIM To study the role of mitochondrial ATP sensitive potassium channels in the myocardial protection associated with the propofol. METHODS Isolated SD rat hearts were perfused by the Langendorff method at a constant flow rate, and left ventricular function and coronary pressure were assessed using standard methods. To assess the role of K ATP channels, hearts were pretreated with the K ATP blocker 5 hydroxydecanoate (5 HD)(100 μmol·L -1 ) and then exposed to either control buffer or buffer containing propofol(100 μmol·L -1 ) or the combination of propofol and 5 HD or buffer containing 5 HD. After stabilization in K H solution for 20 min, the hearts were rendered globally ischemic for 25 min, then reperfusion began with K H solution for 30 min. The left ventricular developed pressure(LVDP) and left ventricular end diastolic pressure( LVEDP) were recorded by the Maclab.The value of MDA was determined at the end of reperfusion. RESULTS The Hearts treated with propofol or propofol plus 5 HD showed significantly higher recovery of left ventricular developed pressure and reduced left ventricular end diastolic pressures compared with the controls ( P <0 05). In contrast, there was no significant differences between porpofol and propofol plus 5 HD ( P >0 05) groups. Whereas there was also no significant differences between control and 5 HD ( P >0 05) group. Treatment with propofol or the combination of propofol and 5 HD delayed the onset of contracture during ischemia compared with control or 5 HD treatments for (6 4±2 1) min or (6 8±2 5) min vs (4 4±1 4) min or (4 2±1 6) min, respectively; P <0 05). At the end of reperfusion, the value of MDA in control, propofol and propofol plus 5 HD and 5 HD was (113 7±20 9), (89 4±13 7), (91 9±14 4) nmol·100 mg -1 and 114 8±19 7 nmol·100 mg -1 ,respectively. The value of MDA in propofol or propofol plus 5 HD was significantly lower than the control or 5 HD group( P <0 05),whereas there was no significant difference between propofol and the combination of propofol and 5 HD( P >0 05). The LVEDP in propofol or propofol plus 5 HD increased more slowly than in the control or 5 HD group. Maximal LVEDP occurred 17 min or 16 min,respectively after ischemia in the control group,whereas it occurred 20 and 22 min after ischemia in propofol and propofol plus 5 HD groups, respectively( P <0 05). Pretreament with 5 HD had no effect on the cardioprotection associated with propofol preconditioning. CONCLUSION Mitochondrial ATP sensitive potassium channels is not in volved in the cardioprotection by propofol preconditioning.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2003年第10期1155-1159,共5页
Chinese Pharmacological Bulletin
