Muravchick Stanley, Levy Richard J
Department of Anesthesiology and Critical Care, Hospital of the University of Pennsylvania, and The Children's Hospital of Philadelphia, 3400 Spruce Street, Philadelphia, PA 19104, USA.
Anesthesiology. 2006 Oct;105(4):819-37. doi: 10.1097/00000542-200610000-00029.
Mitochondria produce metabolic energy, serve as biosensors for oxidative stress, and eventually become effector organelles for cell death through apoptosis. The extent to which these manifold mitochondrial functions are altered by previously unrecognized actions of anesthetic agents seems to explain and link a wide variety of perioperative phenomena that are currently of interest to anesthesiologists from both a clinical and a scientific perspective. In addition, many surgical patients may be at increased perioperative risk because of inherited or acquired mitochondrial dysfunction leading to increased oxidative stress. This review summarizes the essential aspects of the bioenergetic process, presents current knowledge regarding the effects of anesthetics on mitochondrial function and the extent to which mitochondrial state determines anesthetic requirement and potential anesthetic toxicity, and considers some of the many implications that our knowledge of mitochondrial dysfunction poses for anesthetic management and perioperative medicine.
线粒体产生代谢能量,作为氧化应激的生物传感器,并最终通过凋亡成为细胞死亡的效应细胞器。麻醉剂以前未被认识的作用对这些多样的线粒体功能改变的程度,似乎可以解释并联系目前麻醉医生从临床和科学角度都感兴趣的各种围手术期现象。此外,许多外科手术患者可能因遗传性或获得性线粒体功能障碍导致氧化应激增加而使围手术期风险升高。本综述总结了生物能量过程的基本方面,介绍了关于麻醉剂对线粒体功能影响的现有知识,以及线粒体状态在多大程度上决定麻醉需求和潜在麻醉毒性,并探讨了我们对线粒体功能障碍的认识对麻醉管理和围手术期医学的诸多影响。