Takano N
Respir Physiol. 1984 May;56(2):229-35. doi: 10.1016/0034-5687(84)90106-3.
We studied a maximum fall in VE (max delta VE) produced by 20 sec O2 breathing and its percentage of resting VE (reflex hypoxic drive) on 9 menstruating women, in order to examine menstrual phase effect on reflex hypoxic drive. During the luteal phase, resting PAO2 was higher by 4.8 mm Hg and PACO2 was lower by 3.0 mm Hg than during the follicular phase. In spite of these changes in the alveolar gases, reflex hypoxic drive was greater in the luteal phase (14.4%) than in the follicular phase (9.3%). Resting VE in the luteal phase was 7.8% greater than that in the follicular phase. Contribution of the augmented hypoxic drive to the increased resting VE in the luteal phase, calculated as delta (max delta VE)/delta VE (%), was 59 +/- 29% (mean +/- SE). These results suggest that progesterone-induced hyperventilation, as occurs in the luteal phase, is elicited partly by mediating an increase in reflex hypoxic drive which is probably produced centrally even in hyperoxia and hypocapnia, but the role of augmented hypoxic drive is highly variable among subjects.
我们对9名处于月经期的女性进行研究,观察她们在吸入氧气20秒后每分钟通气量的最大降幅(最大ΔVE)及其占静息每分钟通气量的百分比(反射性低氧驱动),以检验月经周期对反射性低氧驱动的影响。与卵泡期相比,黄体期的静息动脉血氧分压(PAO2)高4.8 mmHg,动脉血二氧化碳分压(PACO2)低3.0 mmHg。尽管肺泡气体有这些变化,但黄体期的反射性低氧驱动(14.4%)仍高于卵泡期(9.3%)。黄体期的静息每分钟通气量比卵泡期高7.8%。黄体期低氧驱动增强对静息每分钟通气量增加的贡献,以Δ(最大ΔVE)/ΔVE(%)计算,为59±29%(平均值±标准误)。这些结果表明,黄体期出现的孕酮诱导的过度通气,部分是通过介导反射性低氧驱动的增加而引发的,即使在高氧和低碳酸血症情况下,这种增加可能也是由中枢产生的,但低氧驱动增强在不同个体中的作用差异很大。