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减压病的机械性与缺血性机制

Mechanical vs. ischemic mechanisms for decompression sickness.

作者信息

Hills B A

出版信息

Aviat Space Environ Med. 1979 Apr;50(4):363-7.

PMID:464957
Abstract

We used 20 kangaroo rats to investigate the effect of exposure to low oxygen levels (0.11 Atm 02 inspired partial pressure) prior to decompression from a steady-state condition. This hypoxia was found to afford significant protection against limb bends as simulated in those animals by tail biting. Yet, it potentiated neurologic symptoms compared with a control exposure on air with the same level of nitrogen supersaturation. However the incidence of simulated limb bends in the same animals was the same with hypoxia as with another control exposure at a pressure estimated to give extravascular bubbles of the same size upon decompression. The results are, therefore, consistent with a simple mechanical basis for limb bends, but are difficult to explain by any ischemic mechanism since a general hypoxia exacerbates any pain produced by oxygen deficiency in the tissues. However, the reverse may be true for some forms of neurologic decompression sickness and the two such cases reported here are consistent with that view, although not statistically significant.

摘要

我们使用20只更格卢鼠来研究在从稳态条件减压之前暴露于低氧水平(吸入氧分压为0.11个大气压)的影响。发现这种低氧状态能为这些动物模拟的减压病提供显著保护,通过咬尾巴来模拟。然而,与在相同氮过饱和水平的空气中进行对照暴露相比,它会增强神经症状。不过,在相同动物中,模拟减压病的发生率在低氧状态下与在估计减压时会产生相同大小血管外气泡的另一种对照暴露下是相同的。因此,这些结果与减压病的简单机械基础是一致的,但很难用任何缺血机制来解释,因为一般性低氧会加剧组织中缺氧产生的任何疼痛。然而,对于某些形式的神经减压病情况可能相反,这里报告的两例此类病例与该观点一致,尽管在统计学上不显著。

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