Marczak M, Pokorski M
Department of Respiratory Research, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
J Physiol Pharmacol. 2004 Mar;55(1 Pt 1):127-34.
We investigated the ventilatory response to normobaric poikilocapnic hyperoxia in healthy subjects. The study was carried out in 26 subjects of the mean age 26 +/- 0.9 (SE) years, who breathed pure oxygen through a two-way valve for 10 min. The subjects were in the sitting position with a mouthpiece and nose clip attached. Ventilatory flow was recorded using a pneumotachograph and minute ventilation was calculated from the tidal and frequency components. The SaO(2) and alveolar CO(2) tension were continuously monitored. Ten of the same subjects constituted a control group in which room air was substituted for oxygen and the tests repeated in the same way at another occasion. We found that oxygen breathing caused a transient 8.4% decline in ventilation, whose nadir was 1 min after the introduction of oxygen. Thereafter, ventilation increased significantly above the baseline value and showed a further rising tendency toward the end of the test. We conclude that acute oxygen treatment is unlikely to have a major inhibitory effect on the carotid body-dependent ventilatory drive in normal subjects. The determinants of the hyperoxic ventilatory stimulation remain to be established in further studies.
我们研究了健康受试者对常压变碳酸性高氧的通气反应。该研究在26名平均年龄为26±0.9(标准误)岁的受试者中进行,他们通过双向阀吸入纯氧10分钟。受试者坐在椅子上,佩戴口器和鼻夹。使用呼吸流速计记录通气流量,并根据潮气量和频率成分计算每分钟通气量。连续监测血氧饱和度(SaO₂)和肺泡二氧化碳张力。其中10名相同的受试者组成一个对照组,用室内空气代替氧气,并在另一个时间以相同方式重复测试。我们发现,吸氧导致通气量短暂下降8.4%,其最低点出现在吸氧后1分钟。此后,通气量显著高于基线值,并在测试接近尾声时呈现进一步上升趋势。我们得出结论,急性氧疗不太可能对正常受试者中依赖颈动脉体的通气驱动产生重大抑制作用。高氧通气刺激的决定因素仍有待进一步研究确定。