Akata Takashi
Department of Anesthesiology and Critical Care Medicine, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan.
J Anesth. 2007;21(2):220-31. doi: 10.1007/s00540-006-0487-5. Epub 2007 May 30.
General anesthetics cause hemodynamic instability and alter blood flow to various organs. There is mounting evidence that most general anesthetics, at clinical concentrations, influence a wide variety of cellular and molecular mechanisms regulating the contractile state of vascular smooth muscle cells (i.e., vascular tone). In addition, in current anesthetic practice, various types of vasoactive agents are often used to control vascular reactivity and to sustain tissue blood flow in high-risk surgical patients with impaired vital organ function and/or hemodynamic instability. Understanding the physiological mechanisms involved in the regulation of vascular tone thus would be beneficial for anesthesiologists. This review, in two parts, provides an overview of current knowledge about the cellular and molecular mechanisms regulating vascular tone-i.e., targets for general anesthetics, as well as for vasoactive drugs that are used in intraoperative circulatory management. This first part of the two-part review focuses on basic mechanisms regulating cytosolic Ca2+ concentration and the Ca2+-dependent regulation of vascular tone.
全身麻醉药会导致血流动力学不稳定,并改变流向各个器官的血流。越来越多的证据表明,大多数全身麻醉药在临床浓度下会影响多种调节血管平滑肌细胞收缩状态(即血管张力)的细胞和分子机制。此外,在当前的麻醉实践中,对于重要器官功能受损和/或血流动力学不稳定的高危手术患者,经常使用各种血管活性药物来控制血管反应性并维持组织血流。因此,了解参与血管张力调节的生理机制对麻醉医生来说是有益的。本综述分为两部分,概述了目前关于调节血管张力的细胞和分子机制的知识,即全身麻醉药以及术中循环管理中使用的血管活性药物的作用靶点。这篇两部分综述的第一部分重点关注调节胞质Ca2+浓度的基本机制以及Ca2+依赖性血管张力调节。