阿托伐他汀抗心肌缺血再灌注损伤的作用机制研究  

The mechanism of atorvastatin on the prevention of heart muscle ischemia-reperfusion injury

作　　者：周常青[1] 马捷[1] 

机构地区：[1]山西医科大学第二医院

出　　处：《临床医药实践》2009年第7期488-489,共2页Proceeding of Clinical Medicine

摘　　要：目的：研究阿托伐他汀（ATV）在对心肌缺血再灌注损伤（IRI）的保护效应中，两种ATP依赖的K^＋（KATP）通道的作用。方法：将32只实验家兔随机分为对照组、ATV组、ATV＋5-HD（A1组）、ATV＋HMR1883（A2组）。通过结扎和放松冠状动脉左前降支，分别进行30min的心肌缺血和再灌注。实验中持续监测左室舒张末期压（LVEDP）、左心室压最大变化速率（±dp／dtmax）的变化。结果：与对照组相比：ATV组及A2组各项心功能指标在再灌注30min后明显改善（P〈0．05），而A1组差异无显著性（P〉0．05）。结论：ATV的抗心肌IRI保护效应可能与线粒体KATP通道有关。Objective： To observe the role of two ATP-sensitive K^＋ channels in the protective effect of atorvastatin （ATV）on myocardial ischemia-reperfusion injury（IRI）. Methods ：Thirty-two rabbits were randomly divided into four groups ：control group ,ATV group ,ATV＋5-HD（A1） ,ATV＋HMR1883（A2）. All rabbis were subjected to 30 min ischemia and 30 min reperfusion. The max rate of rise of left ventricular pressure（±dp/dtmax） and left ventricular enddiastolic pressure（LVEDP） were detected during the experiment. Results：Compared with the control group,the indexes of heart function were improved significantly（P〈0.05） in the ATV group and the A2 group. And there was no statistically significant between the control group and A1 group （P〉0. 05）. Conclusion： The mitochondrial KATP channel is likely involved in the protective mechanism that against myocardial IRI in rabbits of ATV.

关 键 词：阿托伐他汀 心肌缺血再灌注损伤 线粒体KATP通道 

分 类 号：R54[医药卫生—心血管疾病]