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惰性气体麻醉的近期神经化学数据综述。

A review of recent neurochemical data on inert gas narcosis.

作者信息

Rostain J C, Lavoute C, Risso J J, Vallée N, Weiss M

机构信息

Université de la Méditerranée et IMNSSA UMR-MD2, Physiologie et Physiopathologie en Condition d'Oxygénation Extrême, Faculté de Médecine Nord, Institut de Neuroscience Jean Roche, 13015 Marseille, France.

出版信息

Undersea Hyperb Med. 2011 Jan-Feb;38(1):49-59.

PMID:21384763
Abstract

Nitrogen narcosis occurs in humans at around 0.4 MPa (4 ATA). Hydrogen narcosis occurs between 2.6 and 3.0 MPa. In rats, nitrogen disturbances occur from 1 MPa and a loss of righting reflex around 4 MPa. Neurochemical studies in striatum of rats with nitrogen at 3 MPa (75% of anesthesia threshold) with differential pulse voltammetry have demonstrated a decrease in dopamine (DA) release by neurons originated from the substantia nigra pars compacta (SNc). Such a decrease is found also with compressed argon, which is more narcotic than nitrogen and with the anesthetic gas nitrous oxide. Inversely, compressed helium with its very low narcotic potency induces DA increase. Microdialysis studies in the striatum have indicated that nitrogen also induces a decrease of glutamate concentration. Nitrogen pressure did not modify NMDA glutamate receptor activities in SNc or striatum but enhanced GABAA receptors activities in SNc. Repetitive exposures to nitrogen narcosis suppressed the DA decrease and induced an increase. This fact and the lack of improvement of motor disturbances did not support the hypothesis of a physiological adaptation. The desensitization of the GABAA receptors on DA cells during recurrent exposures and the parallel long-lasting decrease of glutamate coupled to the increase in NMDA receptor sensitivity suggest a nitrogen neurotoxicity or addiction induced by recurrent exposures. The differential changes produced by inert gases indifferent neurotransmitter receptors would support the binding protein theory.

摘要

氮麻醉在人体中大约在0.4兆帕(4个绝对大气压)时发生。氢麻醉发生在2.6至3.0兆帕之间。在大鼠中,1兆帕时会出现氮干扰,4兆帕左右会出现翻正反射丧失。用差分脉冲伏安法对处于3兆帕(麻醉阈值的75%)氮气环境中的大鼠纹状体进行神经化学研究表明,源自黑质致密部(SNc)的神经元释放的多巴胺(DA)减少。在压缩氩气(比氮气更具麻醉性)和麻醉气体一氧化二氮环境中也发现了这种减少。相反,麻醉效力极低的压缩氦气会导致多巴胺增加。纹状体的微透析研究表明,氮气也会导致谷氨酸浓度降低。氮气压力并未改变SNc或纹状体中NMDA谷氨酸受体的活性,但增强了SNc中GABAA受体的活性。反复暴露于氮麻醉会抑制多巴胺的减少并导致其增加。这一事实以及运动障碍没有改善并不支持生理适应的假设。反复暴露期间DA细胞上GABAA受体的脱敏以及谷氨酸的平行长期减少与NMDA受体敏感性增加表明反复暴露会导致氮神经毒性或成瘾。惰性气体在不同神经递质受体上产生的差异变化将支持结合蛋白理论。

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