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线粒体KATP在阿托伐他汀心功能保护效应中的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2008年第6期
页码:
682-685
栏目:
基础研究
出版日期:
2008-12-25

文章信息/Info

Title:
Effect of mitochondrial KATP on Atovastatin’s cardiac function protection
作者:
陈曼华; 周逸; 刘锦华; 张利芸
武汉市中心医院心血管内科，湖北 武汉430014
Author(s):
CHEN Manhua;  ZHOU Yi;  LIU Jinhua;  ZHANG Liyun
Department of Cardiology, Wuhan Central Hospital, Wuhan 430014, Hubei, China
关键词:
阿托伐他汀; 兔; 心功能; 缺血/再灌注; ATP敏感性钾通道; 线粒体
Keywords:
atovastatin;  rabbits;  cardiac function;  ischemiareperfusion;  ATP sensitive potassium channel;  mitochondrial
分类号:
R972
DOI:
-
文献标识码:
A
摘要:
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40 min局部缺血和240 min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)；3 d ATV 10 mg/(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mito KATP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。
Abstract:
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 subjected to 40min of regional ischemia and 240 min reperfusion. The hemodynamic variables, CKMB, LDH1 and capacity of mitochondrial ATP synthesization (［ATP］m) were determined after reperfusion. 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.

参考文献/References

［1］ Schulz R. Pleiotropic effects of statins: Acutely good, but chronically bad?［J］. J Am Coll Cardiol, 2005, 45(8):1292-1294.

［2］ Gross GJ, Auchampach JA. Blockade of ATPsensitive potassium channels prevents myocardial preconditioning in dogs［J］. Circ Res, 1992, 70(2):223-233.

［3］ Nayler WG, Ferrari R, Williams A. Protective effect of pretreatment with verapamil, nifedipine and propranolol on mitochondrial function in the ischemic and reperfused myocardium［J］. Am J Cardiol, 1980, 46(2):242-248.

［4］ Kawabata H, Ryomoto T, Ishikawa K. Role of cardiac ATPsensitive K+ channels induced by HMG CoA reductase inhibitor in ischemic rabbit hearts［J］. Hypertens Res, 2001, 24(5):573-577.

［5］ Tavackoli S, Ashitkov T, Hu ZY, et al. Simvastatininduced myocardial protection against ischemiareperfusion injury is mediated by activation of ATPsensitive K+ channels［J］. Coron Artery Dis, 2004, 15(1):53-58.

［6］ 周逸,唐其柱. ATP敏感性钾通道在缺血预适应中的作用［J］. 心脏杂志, 2005, 17(1): 83-86.

［7］ Auchampach JA, Grover GJ, Gross GJ. Blockade of ischemic preconditioning in dogs by the novel ATPdependent potassium channel antagonist sodium 5hydroxydecanoate［J］. Cardiovasc Res, 1992, 26(11):1954-1962.

［8］ Sato T, Sasaki N, O’Rourke B, et al. Nicorandil, a potent cardioprotective agent, acts by opening mitochondrial ATPdependent potassium channels［J］. J Am Coll Cardiol, 2000, 35(2):514-518.

［9］ Sasaki N, Murata M, Guo Y, et al. MCC134, a Single Pharmacophore, Opens Surface ATPSensitive Potassium Channels, Blocks Mitochondial ATPSensitive Potassium Channels, and Suppresses Preconditioning［J］. Circulation, 2003, 107(8):1183-1188.

［10］O’Rourke B. Evidence for Mitochondrial K+ Channels and Their Role in cardioprotection［J］. Circ Res, 2004, 94(4):420-432.

［11］Solaini G, Harris DA. Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion［J］. Biochem J, 2005, 390(Pt 2):377-394.

［12］Zhuo ML, Huang Y, Liu DP, et al. KATP channel: relation with cell metabolism and role in the cardiovascular system［J］. Int J Biochem Cell Biol, 2005, 37(4):751-764.

备注/Memo

备注/Memo:
收稿日期：2007-02-15.通讯作者：陈曼华，主任医师，教授，主要从事冠心病的介入 治疗及基础研究Email:sjcmh@yahoo.com.cn
更新日期/Last Update: 2009-03-24