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人体对中度低氧血症的通气适应。脑脊液(H⁺)的作用。

Ventilatory acclimatization to moderate hypoxemia in man. The role of spinal fluid (H+).

作者信息

Dempsey J A, Forster H V, DoPico G A

出版信息

J Clin Invest. 1974 Apr;53(4):1091-100. doi: 10.1172/JCI107646.

DOI:10.1172/JCI107646
PMID:4815077
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC333094/
Abstract

This study has assessed the regulation of arterial blood and cerebrospinal fluid (CSF) pH and thereby their contribution to the control of breathing in normal man during various stages of ventilatory acclimatization to 3,100 m altitude. CSF acid-base status was determined: (a) from measurements of lumbar spinal fluid during steady-state conditions of chronic normoxia (250 m altitude) and at + 8 h and + 3-4 wk of hypobaric hypoxia; and (b) from changes in cerebral venous P(CO2) at + 1 h hypoxic exposure. After 3-4 wk at 3,100 m, CSF [H(+)] remained significantly alkaline to values obtained in either chronic normoxia or with 1 h hypoxic exposure and was compensated to the same extent ( approximately 66%) as was arterial blood [H(+)]. Ventilatory acclimatization to 3,100 m bore no positive relationship to accompanying changes in arterial P(O2) and pH and CSF pH: (a) CSF pH either increased or remained constant at 8 h and at 3-4 wk hypoxic exposure, respectively, coincident with significant, progressive reductions in Pa(CO2); (b) arterial P(O2) and pH increased progressively with time of exposure; and (c) in the steady-state of acclimatization to 3,100 m the combination of chemical stimuli present, i.e. Pa(O2) = 60 mm Hg, pHa and pH(CSF) = + 0.03-0.04 > control, was insufficient to produce the observed hyperventilation (Pa(CO2) = 32 mm Hg). It was postulated that ventilatory acclimatization to 3,100 m altitude was mediated by factors other than CSF [H(+)] and that the combination of chronic hypoxemia and hypocapnia of moderate degrees provided no mechanisms for the specific regulation of CSF [H(CO3) (-)] and hence for homeostasis of CSF [H(+)].

摘要

本研究评估了动脉血和脑脊液(CSF)pH值的调节,从而评估了它们在正常男性对海拔3100米的通气适应的各个阶段中对呼吸控制的贡献。测定了脑脊液的酸碱状态:(a)在慢性常氧(海拔250米)稳态条件下以及低压缺氧8小时和3 - 4周时,通过测量腰椎脑脊液来确定;(b)在缺氧暴露1小时时,通过脑静脉P(CO2)的变化来确定。在海拔3100米处3 - 4周后,脑脊液[H(+)]仍显著呈碱性,与慢性常氧或缺氧暴露1小时时获得的值相比,且与动脉血[H(+)]的补偿程度相同(约66%)。对海拔3100米的通气适应与动脉P(O2)、pH值以及脑脊液pH值的伴随变化没有正相关关系:(a)在缺氧暴露8小时和3 - 4周时,脑脊液pH值分别升高或保持不变,同时动脉血二氧化碳分压(Pa(CO2))显著且逐渐降低;(b)动脉P(O2)和pH值随暴露时间逐渐升高;(c)在对海拔3100米的适应稳态中,存在的化学刺激组合,即动脉血氧分压(Pa(O2)) = 60毫米汞柱,动脉血pH值(pHa)和脑脊液pH值(pH(CSF)) = + 0.03 - 0.04 > 对照,不足以产生观察到的过度通气(Pa(CO2) = 32毫米汞柱)。据推测,对海拔3100米的通气适应是由脑脊液[H(+)]以外的因素介导的,并且中度慢性低氧血症和低碳酸血症的组合没有为脑脊液[H(CO3)(-)]的特异性调节提供机制,因此也没有为脑脊液[H(+)]的稳态提供机制。

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