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人体在等碳酸血症和变碳酸血症性低氧血症48小时期间及之后呼吸控制的变化。

Changes in respiratory control during and after 48 h of isocapnic and poikilocapnic hypoxia in humans.

作者信息

Tansley J G, Fatemian M, Howard L S, Poulin M J, Robbins P A

机构信息

University Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, United Kingdom.

出版信息

J Appl Physiol (1985). 1998 Dec;85(6):2125-34. doi: 10.1152/jappl.1998.85.6.2125.

DOI:10.1152/jappl.1998.85.6.2125
PMID:9843535
Abstract

Ventilatory acclimatization to hypoxia is associated with an increase in ventilation under conditions of acute hyperoxia (VEhyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). This study compares 48-h exposures to isocapnic hypoxia (protocol I) with 48-h exposures to poikilocapnic hypoxia (protocol P) in 10 subjects to assess the importance of hypocapnic alkalosis in generating the changes observed in ventilatory acclimatization to hypoxia. During both hypoxic exposures, end-tidal PO2 was maintained at 60 Torr, with end-tidal PCO2 held at the subject's prehypoxic level (protocol I) or uncontrolled (protocol P). VEhyperoxia and AHVR were assessed regularly throughout the exposures. VEhyperoxia (P < 0.001, ANOVA) and AHVR (P < 0.001) increased during the hypoxic exposures, with no significant differences between protocols I and P. The increase in VEhyperoxia was associated with an increase in slope of the ventilation-end-tidal PCO2 response (P < 0.001) with no significant change in intercept. These results suggest that changes in respiratory control early in ventilatory acclimatization to hypoxia result from the effects of hypoxia per se and not the alkalosis normally accompanying hypoxia.

摘要

通气对低氧的适应与急性高氧条件下通气量的增加(高氧通气量,VEhyperoxia)以及急性低氧通气反应(AHVR)的增强有关。本研究在10名受试者中比较了48小时等碳酸低氧暴露(方案I)与48小时变碳酸低氧暴露(方案P),以评估低碳酸碱中毒在产生通气对低氧适应中所观察到的变化方面的重要性。在两种低氧暴露期间,呼气末PO2维持在60 Torr,呼气末PCO2保持在受试者低氧前水平(方案I)或不加控制(方案P)。在整个暴露过程中定期评估高氧通气量和急性低氧通气反应。在低氧暴露期间,高氧通气量(方差分析,P < 0.001)和急性低氧通气反应(P < 0.001)增加,方案I和P之间无显著差异。高氧通气量的增加与通气-呼气末PCO2反应斜率的增加相关(P < 0.001),截距无显著变化。这些结果表明,通气对低氧适应早期呼吸控制的变化是由低氧本身的作用引起的,而不是通常伴随低氧的碱中毒。

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