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睡眠剥夺和睡眠片段化对正常受试者上气道可塌陷性的影响。

Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects.

作者信息

Sériès F, Roy N, Marc I

机构信息

Unité de recherche, Centre de pneumologie de l'hôpital Laval, Université Laval, Sainte-Foy, Quebec, Canada.

出版信息

Am J Respir Crit Care Med. 1994 Aug;150(2):481-5. doi: 10.1164/ajrccm.150.2.8049833.

DOI:10.1164/ajrccm.150.2.8049833
PMID:8049833
Abstract

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.

摘要

睡眠剥夺可诱发或加重夜间呼吸紊乱。在睡眠呼吸暂停低通气患者中,睡眠异常包括反复出现的觉醒和唤醒发作,导致睡眠片段化。由于这些患者上气道塌陷的倾向增加,我们想知道睡眠片段化是否会增加上气道的可塌陷性,并促成这种疾病的发病机制。在8名正常受试者中,通过在记录气流、面罩压力和食管压力的同时逐渐降低鼻罩中的压力,在睡眠期间评估上气道的可塌陷性。临界压力由每个气流受限吸气周期的最大吸气气流逐次呼吸值与相应的面罩压力之间的关系确定。在每个受试者中测量两次临界压力:在一夜完全睡眠剥夺后和使用听觉刺激进行一夜睡眠片段化后。这两种测量以随机顺序进行,间隔1周。在每次临界压力测量后的晚上进行多导睡眠图记录。睡眠剥夺和睡眠片段化后的睡眠结构相同。与睡眠剥夺后相比,睡眠片段化后与睡眠相关的呼吸异常更频繁。睡眠剥夺后临界压力为-17.1±6.8 cmH₂O(平均值±标准误),睡眠片段化后为-12.3±6.3 cmH₂O(p<0.05),这对应于上气道更早关闭。我们得出结论,与睡眠剥夺相比,睡眠片段化导致更高的上气道可塌陷性。

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