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内耳减压病的生物物理基础。

Biophysical basis for inner ear decompression sickness.

作者信息

Doolette David J, Mitchell Simon J

机构信息

Anaesthesia and Intensive Care, The University of Adelaide, Adelaide 5005, Australia.

出版信息

J Appl Physiol (1985). 2003 Jun;94(6):2145-50. doi: 10.1152/japplphysiol.01090.2002. Epub 2003 Jan 31.

Abstract

Isolated inner ear decompression sickness (DCS) is recognized in deep diving involving breathing of helium-oxygen mixtures, particularly when breathing gas is switched to a nitrogen-rich mixture during decompression. The biophysical basis for this selective vulnerability of the inner ear to DCS has not been established. A compartmental model of inert gas kinetics in the human inner ear was constructed from anatomical and physiological parameters described in the literature and used to simulate inert gas tensions in the inner ear during deep dives and breathing-gas substitutions that have been reported to cause inner ear DCS. The model predicts considerable supersaturation, and therefore possible bubble formation, during the initial phase of a conventional decompression. Counterdiffusion of helium and nitrogen from the perilymph may produce supersaturation in the membranous labyrinth and endolymph after switching to a nitrogen-rich breathing mixture even without decompression. Conventional decompression algorithms may result in inadequate decompression for the inner ear for deep dives. Breathing-gas switches should be scheduled deep or shallow to avoid the period of maximum supersaturation resulting from decompression.

摘要

孤立性内耳减压病(DCS)在涉及呼吸氦氧混合气的深潜中被认识到,特别是在减压过程中呼吸气体切换为富含氮气的混合气时。内耳对减压病这种选择性易损性的生物物理基础尚未确立。根据文献中描述的解剖学和生理学参数构建了人类内耳惰性气体动力学的房室模型,并用于模拟在据报道会导致内耳减压病的深潜和呼吸气体替换过程中内耳中的惰性气体张力。该模型预测在传统减压的初始阶段会有相当程度的过饱和,因此可能形成气泡。即使不进行减压,在切换到富含氮气的呼吸混合气后,来自外淋巴的氦气和氮气的逆向扩散也可能在膜迷路和内淋巴中产生过饱和。传统的减压算法可能导致深潜时内耳减压不足。呼吸气体切换应安排在深度较深或较浅时进行,以避免减压导致的最大过饱和期。

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