线粒体KATP在阿托伐他汀心功能保护效应中的作用

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（mito KATP）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）；3d ATV 10mg／（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，mito KATP是KATP途径的主要作用位点。

Effect of mitochondrial KATP on Atovastatin＇s cardiac function protection

AIM To observe the effect of Atovastatin on ischemia-reperfusion myocardium and to determine the role of mitochondrial ATP sensitive potassium channel （mito KATP） in this effect. METHODS The rabbits for the study were randomly divided into control group, ATV group, ATV ＋ 5-hydroxydecanoate （5-HD） group and 5-HD group. All the rabbits were 240 rain reperfusion. The hemodynamic variables, CK-MB, synthesization （ [ ATP ] m） were determined after reperfusion subjected to 40rain of regional ischemia and LDH-1 and capacity of mitochondrial ATP RESULTS Following ischemia-reperfusion, LVDP and ＋ dp/dtmax decreased significantly （ both P 〈0. 01 ）. The 3-day ATV 10 mg/（ kg · d）preconditioning significantly decreased the reduction of LVDP and ＋ dp/dtmax （ both P 〈 0. 01 ）, decreased CK-MB and LDH-1 but increased [ ATP] m. The reduction of LVDP and ＋ dp/dtmax in ATV ＋5-HD group was similar to that in control group. CK-MB, LDH-1 and [ ATP] m were similar to those in control group. CONCLUSION The ATV preconditioning improves contractile function of left ventricular after ischemia-reperfusion by activating mito KATP. The mito KATP plays a major role in KATp pathway.