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高碳酸血症不影响慢性缺氧引起的功能残气量增大。

Hypercapnia does not affect functional residual capacity enlargement induced by chronic hypoxia.

作者信息

Maxová H, Vízek M

机构信息

Institute of Pathological Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic.

出版信息

Physiol Res. 2002;51(5):537-40.

Abstract

To determine whether changes in partial pressure of CO2 participate in mechanism enlarging the lung functional residual capacity (FRC) during chronic hypoxia, we measured FRC and ventilation in rats exposed either to poikilocapnic (group H, F(I)O2 0.1, F(I)CO2 <0.01) or hypercapnic (group H+CO2, F(I)O2 0.1, F(I)CO2 0.04-0.05) hypoxia for the three weeks and in the controls (group C) breathing air. At the end of exposure a body plethysmograph was used to measure ventilatory parameters (V'(E), f(R), V(T)) and FRC during air breathing and acute hypoxia (10 % O2 in N2). The exposure to hypoxia for three weeks increased FRC measured during air breathing in both experimental groups (H: 3.0+/-0.1 ml, H+CO2: 3.1+/-0.2 ml, C: 1.8+/-0.2 ml). During the following acute hypoxia, we observed a significant increase of FRC in the controls (3.2+/-0.2 ml) and in both experimental groups (H: 3.5+/-0.2 ml, H+CO2: 3.6+/-0.2 ml). Because chronic hypoxia combined with chronic hypercapnia and chronic poikilocapnic hypoxia induced the same increase of FRC, we conclude that hypercapnia did not participate in the FRC enlargement during chronic hypoxia.

摘要

为了确定二氧化碳分压的变化是否参与慢性低氧期间肺功能残气量(FRC)增大的机制,我们测量了暴露于变碳酸血症(H组,吸入氧分数(F(I)O2)0.1,吸入二氧化碳分数(F(I)CO2)<0.01)或高碳酸血症(H + CO2组,F(I)O2 0.1,F(I)CO2 0.04 - 0.05)低氧环境三周的大鼠以及呼吸空气的对照组(C组)的FRC和通气情况。在暴露结束时,使用体容积描记器测量在呼吸空气和急性低氧(氮气中10%氧气)期间的通气参数(每分钟静息通气量(V'(E))、呼吸频率(f(R))、潮气量(V(T)))和FRC。暴露于低氧环境三周增加了两个实验组在呼吸空气时测量的FRC(H组:3.0±0.1 ml,H + CO2组:3.1±0.2 ml,C组:1.8±0.2 ml)。在随后的急性低氧期间,我们观察到对照组(3.2±0.2 ml)以及两个实验组(H组:3.5±0.2 ml,H + CO2组:3.6±0.2 ml)的FRC显著增加。由于慢性低氧合并慢性高碳酸血症和慢性变碳酸血症低氧诱导了相同程度的FRC增加,我们得出结论,高碳酸血症不参与慢性低氧期间FRC的增大。

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