Effect of different levels of hyperoxia on breathing in healthy subjects
Effect of different levels of hyperoxia on breathing in healthy subjects
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DOI：
10.1152/jappl.1996.81.4.1683
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发表时间：
1996-10-01
影响因子：
3.3
通讯作者：
Sullivan, CE
中科院分区：
文献类型：
--
作者：
Becker, HF;Polo, O;Sullivan, CE
我们最近表明，如果维持呼气末 PCO2 (PET(CO2))，则呼吸 50% O-2 可显着刺激健康受试者的通气。本研究的目的是调查 O-2 对通气可能的剂量依赖性刺激，并检查高氧过度通气的可能机制。在 8 名正常受试者呼吸 30% 和 75% O-2 30 分钟时测量通气量，PET(CO2) 保持恒定。还测试了这些受试者的急性高碳酸血症通气反应。在 14 名受试者中重复进行 75% O-2 实验，不控制 PET(CO2)，并在基线和高氧期结束时对 6 名受试者进行动脉血气分析。在等碳酸高氧浓度为 30% 和 75% 时，每分钟通气量（V 相对于 I 点）分别增加 21% 和 115%。对 PET(CO2) 没有任何控制的 75% O-2 导致 V 比点 I 增加 16%，但 PET(CO2) 降低了 3.6 Torr (9%)。高碳酸血症和高氧通气反应之间存在线性相关性（r = 0.83）。总之，等二氧化碳高氧以剂量依赖性方式刺激通气，75% O-2 30 分钟后 V 超过点 I 增加一倍多。如果不能维持等碳酸血症，过度通气会因动脉 PCO2 的减少而减弱。高氧和高碳酸血症通气反应之间存在相关性。根据文献数据，我们得出结论，霍尔丹效应似乎是等二氧化碳和异二氧化碳高氧期间过度通气的主要原因。
We have recently shown that breathing 50% O-2 markedly stimulates ventilation in healthy subjects if end-tidal PCO2 (PET(CO2)) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O-2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O-2 for 30 min, with PET(CO2) being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O-2 experiment was repeated without controlling PET(CO2) in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (V over dot I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O-2 without any control on PET(CO2) led to a 16% increase in V over dot I, but PET(CO2) decreased by 3.6 Torr (9%). There was a linear correlation (r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, with V over dot I more than doubling after 30 min of 75% O-2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial PCO2. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.