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吡那地尔对心肌保护作用机制的研究进展
引用本文:彭念寅,周红,司良毅. 吡那地尔对心肌保护作用机制的研究进展[J]. 中国药理学通报, 2004, 20(6): 605-608
作者姓名:彭念寅  周红  司良毅
作者单位:1. 第三军医大学西南医院老年病科,重庆,400038
2. 第三军医大学西南医院药理学教研室,重庆,400038
基金项目:国家重点基础研究发展计划(973计划)
摘    要:近年来研究发现 ,吡那地尔对心肌产生保护作用的靶点是心肌线粒体内膜K(ATP)通道〔mitoK(ATP)〕 ,但是这种缺血预适应的保护作用的机制仍然没有清楚。该文对吡那地尔作用于心肌mitoK(ATP)通道的特征和机制作了进一步的阐述。

关 键 词:吡那地尔  线粒体ATP敏感性K+通道  心肌
文章编号:1001-1978(2004)06-0605-04
修稿时间:2003-12-03

Recent progress and propect in the studies of pinacidil roles on myocardial protection
PENG Nian-Yin,ZHOU Hong,SI Liang-Yi. Recent progress and propect in the studies of pinacidil roles on myocardial protection[J]. Chinese Pharmacological Bulletin, 2004, 20(6): 605-608
Authors:PENG Nian-Yin  ZHOU Hong  SI Liang-Yi
Affiliation:PENG Nian-Yin,ZHOU Hong1,SI Liang-Yi
Abstract:In recent years, it was found that heart was significantly protected against ischemia-reperfusion injury if it was first preconditioned by brief ischemia or by administering a potassium channel opener. Both of these preconditioning strategies were found to require opening of a K(ATP) channel, we showed that this pivotal role was mediated by the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)). As the mechanism was not clarified yet, this paper reviewed the evidence showing that the mechanism and the characters of mito K(ATP) and its cardioprotection against ischemia-reperfusion injury
Keywords:myocardium  pinacidil  mitochondria
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