Suppr超能文献

睡眠及睡眠剥夺对支气管收缩通气反应的影响。

Effect of sleep and sleep deprivation on ventilatory response to bronchoconstriction.

作者信息

Ballard R D, Tan W C, Kelly P L, Pak J, Pandey R, Martin R J

机构信息

Department of Medicine, Veterans Administration Medical Center, Denver, Colorado.

出版信息

J Appl Physiol (1985). 1990 Aug;69(2):490-7. doi: 10.1152/jappl.1990.69.2.490.

Abstract

To characterize ventilatory responses to bronchoconstriction during sleep and to assess the effect of prior sleep deprivation on ventilatory and arousal responses to bronchoconstriction, bronchoconstriction was induced in eight asthmatic subjects while they were awake, during normal sleep, and during sleep after a 36-h period of sleep deprivation. Each subject was bronchoconstricted with increasing concentrations of aerosolized methacholine while ventilatory patterns and lower airway resistance (Rla) were continually monitored. The asthmatic patients maintained their minute ventilation as Rla increased under all conditions, demonstrating a stable tidal volume with a mild increase in respiratory frequency. Inspiratory drive, as measured by occlusion pressure (P0.1), increased progressively and significantly as Rla increased under all conditions (slopes of P0.1 vs. Rla = 0.249, 0.112, and 0.154 for awake, normal sleep, and sleep after sleep deprivation, respectively, P less than 0.0006). Chemostimuli did not appear to contribute significantly to the observed increases in P0.1. Prior sleep deprivation had no effect on ventilatory and P0.1 responses to bronchoconstriction but did significantly raise the arousal threshold to induced bronchoconstriction. We conclude that ventilatory responses to bronchoconstriction, unlike extrinsic loading, are not imparied by the presence of sleep, nor are they chemically mediated. However, prior sleep deprivation does increase the subsequent arousal threshold.

摘要

为了描述睡眠期间对支气管收缩的通气反应,并评估先前睡眠剥夺对支气管收缩的通气和觉醒反应的影响,在8名哮喘患者清醒时、正常睡眠期间以及36小时睡眠剥夺后的睡眠期间诱导支气管收缩。在持续监测通气模式和气道阻力(Rla)的同时,用浓度递增的雾化乙酰甲胆碱使每位受试者发生支气管收缩。在所有情况下,随着Rla增加,哮喘患者均维持其分钟通气量,表现为潮气量稳定,呼吸频率略有增加。通过阻断压(P0.1)测量的吸气驱动力在所有情况下均随着Rla增加而逐渐显著增加(清醒、正常睡眠和睡眠剥夺后睡眠状态下P0.1与Rla的斜率分别为0.249、0.112和0.154,P<0.0006)。化学刺激似乎对观察到的P0.1增加没有显著贡献。先前的睡眠剥夺对支气管收缩的通气和P0.1反应没有影响,但确实显著提高了对诱导支气管收缩的觉醒阈值。我们得出结论,与外在负荷不同,对支气管收缩的通气反应不会因睡眠而受损,也不是由化学介导的。然而,先前的睡眠剥夺确实会增加随后的觉醒阈值。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验