Takeo S, Nasa Y
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Hachioji, Japan.
Cardiovasc Res. 1999 Jul;43(1):32-43. doi: 10.1016/s0008-6363(99)00079-6.
A brief period of ischemia and reperfusion has been shown to protect the myocardium against subsequent sustained ischemia and reperfusion injury, which is called "preconditioning". A great number of investigators have explored the mechanisms underlying this preconditioning-induced cardioprotection. This article dealt with possible mechanisms of energy metabolism and mitochondrial activity for preconditioning-induced cardioprotection. Particularly, the contribution of energy metabolites produced during a brief period of ischemia and reperfusion injury, as well as mitochondrial function that is modified by changes in mitochondrial ATPase activity, opening of mitochondrial ATP-dependent potassium channels and production of free radicals in mitochondria, to ischemic preconditioning is discussed.
短暂的缺血和再灌注已被证明可保护心肌免受随后的持续性缺血和再灌注损伤，这被称为“预处理”。大量研究人员探讨了这种预处理诱导的心脏保护作用的潜在机制。本文探讨了预处理诱导心脏保护作用的能量代谢和线粒体活性的可能机制。特别讨论了短暂缺血和再灌注损伤期间产生的能量代谢产物的作用，以及线粒体ATP酶活性变化、线粒体ATP依赖性钾通道开放和线粒体自由基产生所改变的线粒体功能对缺血预处理的作用。
