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全身麻醉通过对离子通道的作用介导。

General anesthesia mediated by effects on ion channels.

作者信息

Zhou Cheng, Liu Jin, Chen Xiang-Dong

机构信息

Cheng Zhou, Jin Liu, Xiang-Dong Chen, Department of Anesthesiology, Laboratory of Anesthesia and Critical Care Medicine, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China.

出版信息

World J Crit Care Med. 2012 Jun 4;1(3):80-93. doi: 10.5492/wjccm.v1.i3.80.

DOI:10.5492/wjccm.v1.i3.80
PMID:24701405
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3953864/
Abstract

Although it has been more than 165 years since the first introduction of modern anesthesia to the clinic, there is surprisingly little understanding about the exact mechanisms by which general anesthetics induce unconsciousness. As a result, we do not know how general anesthetics produce anesthesia at different levels. The main handicap to understanding the mechanisms of general anesthesia is the diversity of chemically unrelated compounds including diethyl ether and halogenated hydrocarbons, gases nitrous oxide, ketamine, propofol, benzodiazepines and etomidate, as well as alcohols and barbiturates. Does this imply that general anesthesia is caused by many different mechanisms Until now, many receptors, molecular targets and neuronal transmission pathways have been shown to contribute to mechanisms of general anesthesia. Among these molecular targets, ion channels are the most likely candidates for general anesthesia, in particular γ-aminobutyric acid type A, potassium and sodium channels, as well as ion channels mediated by various neuronal transmitters like acetylcholine, amino acids amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid or N-methyl-D-aspartate. In addition, recent studies have demonstrated the involvement in general anesthesia of other ion channels with distinct gating properties such as hyperpolarization-activated, cyclic- nucleotide-gated channels. The main aim of the present review is to summarize some aspects of current knowledge of the effects of general anesthetics on various ion channels.

摘要

尽管现代麻醉技术首次应用于临床已过去165多年,但令人惊讶的是,对于全身麻醉药诱导意识丧失的确切机制,人们了解甚少。因此,我们并不清楚全身麻醉药在不同层面是如何产生麻醉作用的。理解全身麻醉机制的主要障碍在于化学结构不相关的化合物种类繁多,包括乙醚、卤代烃、气体氧化亚氮、氯胺酮、丙泊酚、苯二氮䓬类药物和依托咪酯,以及醇类和巴比妥类药物。这是否意味着全身麻醉是由多种不同机制引起的?到目前为止,许多受体、分子靶点和神经传递途径已被证明与全身麻醉机制有关。在这些分子靶点中,离子通道最有可能是全身麻醉的作用靶点,特别是A型γ-氨基丁酸、钾离子和钠离子通道,以及由各种神经递质介导的离子通道,如乙酰胆碱、氨基酸氨基-3-羟基-5-甲基-4-异恶唑丙酸或N-甲基-D-天冬氨酸。此外,最近的研究表明,具有不同门控特性的其他离子通道,如超极化激活的环核苷酸门控通道,也参与了全身麻醉过程。本综述的主要目的是总结目前关于全身麻醉药对各种离子通道影响的一些知识要点。

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本文引用的文献

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Isoflurane inhibits the tetrodotoxin-resistant voltage-gated sodium channel Nav1.8.异氟烷抑制抗河豚毒素的电压门控钠通道Nav1.8。
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