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[吸入性麻醉剂对脊髓感觉传导的抑制作用]

[Inhibitory action of sensory transmission by inhalational anesthetics in the spinal cord].

作者信息

Yamauchi Masanori, Omote Keiichi, Namiki Akiyoshi, Collins J G

机构信息

Department of Anesthesiology, Yale University School of Medicine, 06520-8051, USA.

出版信息

Masui. 2003 Mar;52(3):240-50.

Abstract

This review article focuses on the suppression of sensory transmission by inhalational anesthetics at the spinal cord level. Volatile anesthetics (e.g. halothane and isoflurane) suppress neuronal responses evoked by both noxious and non-noxious stimuli. This suppression is mediated largely by activation of GABAA and glycine receptors systems in the spinal dorsal horn. Depression of spinal glutamate receptor systems is also probably involved. The analgesic action of nitrous oxide is produced by activation of supra-spinal descending inhibitory systems, not by direct action on the spinal cord. Activation of the descending inhibitory systems by nitrous oxide causes release of noradrenaline in the spinal dorsal horn, and activates alpha 2 adrenergic receptor systems, resulting in depression of neuronal responses evoked by noxious stimuli. GABAA and glycine receptor systems in the spinal dorsal horn are also important components of nitrous oxide anesthesia in depressing neuronal responses evoked by non-noxious stimuli. Although excitation or inhibition of GABAA, glycine, alpha 2 adrenergic and glutamate receptors systems is an important action of inhalational anesthetics, influence of inhalational anesthetics on interactions among these receptor systems has yet to be studied.

摘要

这篇综述文章聚焦于吸入性麻醉药在脊髓水平对感觉传导的抑制作用。挥发性麻醉药(如氟烷和异氟烷)可抑制由伤害性和非伤害性刺激诱发的神经元反应。这种抑制作用主要是通过激活脊髓背角的GABAA和甘氨酸受体系统介导的。脊髓谷氨酸受体系统的抑制可能也参与其中。氧化亚氮的镇痛作用是通过激活脊髓上的下行抑制系统产生的,而非直接作用于脊髓。氧化亚氮激活下行抑制系统会导致脊髓背角去甲肾上腺素释放,并激活α2肾上腺素能受体系统,从而抑制由伤害性刺激诱发的神经元反应。脊髓背角的GABAA和甘氨酸受体系统也是氧化亚氮麻醉抑制非伤害性刺激诱发的神经元反应的重要组成部分。尽管对GABAA、甘氨酸、α2肾上腺素能和谷氨酸受体系统的兴奋或抑制是吸入性麻醉药的重要作用,但吸入性麻醉药对这些受体系统之间相互作用的影响尚未得到研究。

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