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在等碳酸血症性和变碳酸血症性低氧血症8小时期间及之后,人体对急性高氧的通气反应。

Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia.

作者信息

Tansley J G, Clar C, Pedersen M E, Robbins P A

机构信息

Laboratory of Physiology, University of Oxford, United Kingdom.

出版信息

J Appl Physiol (1985). 1997 Feb;82(2):513-9. doi: 10.1152/jappl.1997.82.2.513.

Abstract

During 8 h of either isocapnic or poikilocapnic hypoxia, there may be a rise in ventilation (VE) that cannot be rapidly reversed with a return to higher PO2 (L. S. G. E. Howard and P. A. Robbins. J. Appl. Physiol. 78:1098-1107, 1995). To investigate this further, three protocols were compared: 1) 8-h isocapnic hypoxia [end-tidal PCO2 (PETCO2) held at prestudy value, end-tidal PO2 (PETO2) = 55 Torr], followed by 8-h isocapnic euoxia (PETO2 = 100 Torr); 2) 8-h poikilocapnic hypoxia followed by 8-h poikilocapnic euoxia; and 3) 16-h air-breathing control. Before and at intervals throughout each protocol, the VE response to eucapnic hyperoxia (PETCO2 held 1-2 Torr above prestudy value, PETO2 = 300 Torr) was determined. There was a significant rise in hyperoxic VE over 8 h during both forms of hypoxia (P < 0.05, analysis of variance) that persisted during the subsequent 8-h euoxic period (P < 0.05, analysis of variance). These results support the notion that an 8-h period of hypoxia increases subsequent hyperoxic VE, even if acid-base changes have been minimized through maintenance of isocapnia during the hypoxic period.

摘要

在8小时的等碳酸血症或变碳酸血症性低氧过程中,通气量(VE)可能会升高,且当恢复到较高的PO2时,这种升高不能迅速逆转(L. S. G. E. Howard和P. A. Robbins. 《应用生理学杂志》78:1098 - 1107, 1995)。为了进一步研究这一现象,比较了三种方案:1)8小时等碳酸血症性低氧[呼气末PCO2(PETCO2)维持在研究前的值,呼气末PO2(PETO2) = 55 Torr],随后是8小时等碳酸血症性常氧(PETO2 = 100 Torr);2)8小时变碳酸血症性低氧,随后是8小时变碳酸血症性常氧;3)16小时空气呼吸对照。在每个方案之前及整个过程中的不同时间点,测定了对常碳酸血症性高氧(PETCO2维持在比研究前的值高1 - 2 Torr,PETO2 = 300 Torr)的VE反应。在两种低氧形式下,高氧通气量在8小时内均显著升高(方差分析,P < 0.05),且在随后的8小时常氧期仍持续存在(方差分析,P < 0.05)。这些结果支持这样一种观点,即8小时的低氧期会增加随后的高氧通气量,即使在低氧期通过维持等碳酸血症使酸碱变化最小化。

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