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正常受试者气道对低碳酸血症反应的模式及机制

Pattern and mechanism of airway response to hypocapnia in normal subjects.

作者信息

O'Cain C F, Hensley M J, McFadden E R, Ingram R H

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1979 Jul;47(1):8-12. doi: 10.1152/jappl.1979.47.1.8.

Abstract

We examined the bronchoconstriction produced by airway hypocapnia in normal subjects. Maximal expiratory flow at 25% vital capacity on partial expiratory flow-volume (PEFV) curves fell during hypocapnia both on air and on an 80% helium- 20% oxygen mixture. Density dependence also fell, suggesting predominantly small airway constriction. The changes seen on PEFV curves were not found on maximal expiratory flow-volume curves, indicating the inhalation to total lung capacity substantially reversed the constriction. Pretreatment with a beta-sympathomimetic agent blocked the response, whereas atropine pretreatment did not, suggesting that hypocapnia affects airway smooth muscle directly, not via cholinergic efferents.

摘要

我们研究了正常受试者气道低碳酸血症所产生的支气管收缩情况。在部分呼气流量-容积(PEFV)曲线上,肺活量25%时的最大呼气流量在低碳酸血症期间,无论是在空气环境还是在80%氦气-20%氧气混合气体环境中均下降。密度依赖性也下降,提示主要是小气道收缩。在最大呼气流量-容积曲线上未发现PEFV曲线上出现的变化,这表明吸入至肺总量可基本逆转这种收缩。用β-拟交感神经药预处理可阻断该反应,而阿托品预处理则不能,这表明低碳酸血症直接影响气道平滑肌,而非通过胆碱能传出神经。

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