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[潜水:气压与神经化学机制]

[Diving: barometric pressure and neurochemical mechanisms].

作者信息

Rostain Jean-Claude, Balon Norbert

机构信息

Université de la Méditerranée, Institut de Médecine Navale du Service de Santé des Armées EA3280, Physiopathologie et Action Thérapeutique des Gaz sous Pression, IFR Jean Roche, Faculté de Médecine Nord, Marseille, France.

出版信息

J Soc Biol. 2006;200(3):257-63. doi: 10.1051/jbio:2006030.

Abstract

The studies of Paul Bert, presented in his book "La Pression Barométrique" in 1878, were at the origin of the modern hyperbaric physiology. Indeed his research demonstrated the effects of oxygen at high pressure, that compression effects must be dissociated from decompression effects, and that neurological troubles and death of divers during or after decompression were due to the fast rate of decompression. However, it is only in 1935 that the work of Behnke et al. attributed the complaints reported at 3 bars and above in compressed air or nitrogen-oxygen mixture to the increase in partial pressure of nitrogen which induces nitrogen narcosis. Little is known about the origins and mechanisms of this narcosis. The traditional view was that anaesthesia or narcosis occurred when the volume of a hydrophobic membrane site was caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect during general anaesthesia has long supported this lipid theory. However, recently, protein theories have met with increasing recognition since results with gaseous anaesthetics have been interpreted as evidence for a direct gas-protein interaction. The question is to know whether inert gases, that disrupt dopamine and GABA neurotransmissions and probably glutamatergic neurotransmission, act by binding to neurotransmitter protein receptors.

摘要

保罗·贝尔特于1878年在其著作《气压》中发表的研究,是现代高压生理学的起源。实际上,他的研究证明了高压下氧气的作用,即压缩效应必须与减压效应区分开来,以及潜水员在减压过程中或减压后出现的神经问题和死亡是由于减压速度过快。然而,直到1935年,贝恩克等人的研究才将在3个大气压及以上的压缩空气或氮氧混合物中报告的不适归因于氮分压的增加,这种增加会导致氮麻醉。关于这种麻醉的起源和机制,人们知之甚少。传统观点认为,当麻醉气体分子的吸收导致疏水膜位点的体积膨胀超过临界量时,就会发生麻醉或中毒。全身麻醉期间压力反转效应的观察长期以来一直支持这种脂质理论。然而,最近,蛋白质理论越来越受到认可,因为气态麻醉剂的研究结果被解释为气体与蛋白质直接相互作用的证据。问题在于,惰性气体通过与神经递质蛋白受体结合来干扰多巴胺和GABA神经传递,可能还会干扰谷氨酸能神经传递,情况是否如此。

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