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目的观察阿托伐他汀(ATV)对心肌缺血/再灌注损伤的影响以及线粒体ATP敏感性钾通道(mitoKATP)在其中的作用。方法将兔随机分成缺血/再灌注模型对照组(control组)、ATV组、ATV+5-羟癸酸(5-HD)组、5-HD组。进行40min局部缺血和240min再灌注,观察各组血流动力学、血液生物化学、线粒体ATP合成能力([ATP]m)。结果缺血/再灌注使左室发展压(LVDP)和压力上升最大速率(+dp/dtmax)均显著下降(均P<0.01);3dATV10mg/(kg·d)预处理使缺血/再灌注后LVDP和+dp/dtmax的下降幅度显著降低(均P<0.01),并且降低CK-MB和LDH-1、提高[ATP]m;ATV+5-HD组LVDP和+dp/dtmax的下降幅度、CK-MB、LDH-1、[ATP]m均和对照组无明显差异。结论ATV预处理通过激活mitoKATP改善缺血/再灌注后左室收缩功能,mitoKATP是KATP途径的主要作用位点。
Objective To investigate the effect of atorvastatin (ATV) on myocardial ischemia / reperfusion injury and the role of mitoK ATP in mitochondria. Methods Rabbits were randomly divided into 4 groups: control group, ATV group, ATV + 5-HD group and 5-HD group. 40min ischemia and 240min reperfusion were performed. The hemodynamics, blood biochemistry and mitochondrial ATP synthesis ability ([ATP] m) of each group were observed. Results LVDP and + dp / dtmax decreased significantly after ischemia / reperfusion (all P <0.01). Pretreatment with 3dATV 10 mg / (kg · d) increased ischemia / reperfusion The decrease of LVDP and + dp / dtmax was significantly decreased (both P <0.01), and the decrease of CK-MB and LDH-1 and the increase of [ATP] m in ATV + 5-HD group were also observed , CK-MB, LDH-1, [ATP] m and control group no significant difference. Conclusions ATV preconditioning can improve left ventricular systolic function after ischemia / reperfusion by activating mitoKATP, and mitoKATP is the main site of KATP pathway.