Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics.
Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics.
复制标题
挥发性麻醉剂的心脏预处理：改变线粒体生物能学的决定性作用。
DOI：
10.1089/152308604322899512
复制
发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Kevin,LeoG
中科院分区：
文献类型：
--
作者：
Stowe,DavidF;Kevin,LeoG
挥发性麻醉剂，如氟烷、异氟烷和七氟烷，是最常用于维持全身麻醉状态的药物。人们早就知道它们可以提供一些针对心脏缺血和再灌注影响的保护作用。多种机制可能有助于这种心脏保护，包括冠状血管舒张、收缩力降低以及代谢需求相应减少，以及通过 L 型 Ca2+ 通道减少心肌 Ca2+ 进入的直接作用。最近，这些药物观察到了心脏保护的记忆阶段，该记忆阶段被 ATP 敏感的钾通道抑制所抑制。这些特征表明，尽管这两种刺激之间存在显着差异，但与缺血预处理所需的途径共享成分的途径，并且已采用术语麻醉预处理（APC）。活性氧 (ROS) 清除剂会消除 APC，表明麻醉剂会导致 ROS 形成。这种效果最近已被直接证明。这些药物诱导 ROS 形成的机制尚不清楚。然而，线粒体电子传递系统酶的直接抑制，以及挥发性麻醉剂预处理心脏中线粒体生物能的改变，强烈暗示线粒体是这些效应的目标。此外，在挥发性麻醉剂预处理的心脏缺血和再灌注过程中，线粒体ROS形成减少可能是缺血后结构和功能改善的基础。 APC 提供了一种对人类心脏进行预处理的安全模式。这篇综述总结了这个令临床医生和基础科学家都兴奋的领域的主要进展。
Volatile anesthetic agents, such as halothane, isoflurane, and sevoflurane, are the drugs most commonly used to maintain the state of general anesthesia. They have long been known to provide some protection against the effects of cardiac ischemia and reperfusion. Several mechanisms likely contribute to this cardioprotection, including coronary vasodilation, reduced contractility with corresponding decreased metabolic demand, and a direct effect to decrease myocardial Ca2+entry through L-type Ca2+channels. Recently, a memory phase to cardioprotection has been observed by these agents, which is inhibited by ATP-sensitive potassium channel inhibition. These features suggest a pathway that shares components with those required for ischemic preconditioning, despite the remarkable differences between these two stimuli, and the term anesthetic preconditioning (APC) has been adopted. Scavengers of reactive oxygen species (ROS) abrogate APC, suggesting an effect of anesthetic agents to cause ROS formation. Such an effect has recently been directly demonstrated. The mechanism by which these drugs induce ROS formation is unclear. However, direct inhibition of mitochondrial electron transport system enzymes, and altered mitochondrial bioeneregtics in hearts preconditioned by volatile anesthetics, strongly implicate the mitochondria as the target for these effects. Furthermore, decreased mitochondrial ROS formation during ischemia and reperfusion in hearts preconditioned by volatile anesthetics might underlie the improved postischemic structure and function. APC presents a safe mode to apply preconditioning to human hearts. This review summarizes the major developments in a field that is exciting to clinicians and basic scientists alike.