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月经周期中过度通气后呼吸增强的时间进程变化。

Change in time course of posthyperventilation hyperpnea during menstrual cycle.

作者信息

Takano N

机构信息

Department of School Health, Faculty of Education, Kanazawa University, Japan.

出版信息

J Appl Physiol (1985). 1988 Jun;64(6):2631-5. doi: 10.1152/jappl.1988.64.6.2631.

Abstract

Ventilatory response after 1 min of voluntary hyperventilation (HV) was studied in 10 healthy women. Before, during, and after HV, end-tidal PCO2 (PETCO2) was maintained at a given level between resting and 60 Torr. After cessation of HV, hyperpnea was seen in 179 out of a total of 195 runs but in the remaining 16 runs in 3 subjects hypopnea occurred, both ventilatory changes being followed by slow recovery to the pre-HV level. The time constant (tau) of the decay process of post-HV hyperpnea was calculated and compared between the follicular (F) and luteal (L) phases of menstruation. For post-HV hypopnea, tau was assumed to be zero. There was an inverse correlation between tau and PETCO2 during the test, the relation being similar in F and L. With a phase change from F to L, tau value at resting PETCO2 increased from 17.7 to 23.7 s. Resting PETCO2 decreased from 40.8 to 37.7 Torr, and minute ventilation (VE) increased by 10%. The increased tau in L was ascribable to the decrease in resting PETCO2 but not to the increased ventilatory activity during the pre-HV period (corresponding to the resting VE) that was probably produced by ventilatory stimulation with progesterone in L. From these results, it is inferred that the ventilatory influence of progesterone might not be exerted on the brain stem, which has been implicated as a locus of the afterdischarge mechanism.

摘要

对10名健康女性进行了研究,观察她们在自愿过度通气(HV)1分钟后的通气反应。在HV之前、期间和之后,呼气末二氧化碳分压(PETCO2)维持在静息水平至60托之间的给定水平。在停止HV后,在总共195次测试中,有179次出现了呼吸急促,但在3名受试者的其余16次测试中出现了呼吸不足,两种通气变化之后均缓慢恢复到HV前水平。计算了HV后呼吸急促衰减过程的时间常数(tau),并在月经周期的卵泡期(F)和黄体期(L)之间进行了比较。对于HV后呼吸不足的情况,tau假定为零。测试期间tau与PETCO2呈负相关,F期和L期的关系相似。随着从F期到L期的转变,静息PETCO2时的tau值从17.7秒增加到23.7秒。静息PETCO2从40.8托降至37.7托,分钟通气量(VE)增加了10%。L期tau的增加归因于静息PETCO2的降低,而不是HV前期(对应于静息VE)通气活动的增加,后者可能是由L期孕酮的通气刺激产生的。从这些结果可以推断,孕酮的通气影响可能不会作用于脑干,而脑干被认为是后放电机制的一个部位。

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