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阿托伐他汀抗心肌缺血再灌注损伤的作用机制研究
引用本文:周常青,马捷. 阿托伐他汀抗心肌缺血再灌注损伤的作用机制研究[J]. 临床医药实践, 2009, 18(7): 488-489
作者姓名:周常青  马捷
作者单位:山西医科大学第二医院,山西,太原,030001
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30 min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30 min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.

关 键 词:阿托伐他汀  心肌缺血再灌注损伤  线粒体KATP通道

The mechanism of atorvastatin on the prevention of heart muscle ischemia-reperfusion injury
ZHOU Chang-qing,MA Jie. The mechanism of atorvastatin on the prevention of heart muscle ischemia-reperfusion injury[J]. Proceeding of Clinical Medicine, 2009, 18(7): 488-489
Authors:ZHOU Chang-qing  MA Jie
Abstract: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 end-diastolic 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.
Keywords:atorvastatin  myocardial ischemia-reperfusion  ATP-sensitive K+channels
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