Cala S J, Sliwinski P, Cosio M G, Kimoff R J
Desmond N. Stoker Sleep Laboratory, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
J Appl Physiol (1985). 1996 Dec;81(6):2618-26. doi: 10.1152/jappl.1996.81.6.2618.
It has previously been reported that the duration of obstructive apneas increases from the beginning to the end of the night (M. Charbonneau, J. M. Marin, A. Olha, R. J. Kimoff, R. D. Levy, and M. Cosio. Chest 106: 1695-1701, 1994). The purpose of this study was to test the hypothesis that stimulation of upper airway (UA) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening. We studied seven patients (six men, one woman) with severe obstructive sleep apnea (apnea-hypopnea index = 93 +/- 26 events/h) during two consecutive nights of polysomnographic monitoring. On one night (random order), we performed topical UA anesthesia with 0.2% tetracaine and on the control night, sham anesthesia. We measured apnea duration, esophageal pressure (Pes) during apneas, and apneic O2 desaturation. Consistent with previous findings, apnea duration, number of efforts per apnea, and peak Pes at end apnea increased from the beginning to the end of the control nights. UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night. Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights, but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights. These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal, leading to apnea prolongation.
此前已有报道称，阻塞性呼吸暂停的持续时间从夜间开始到结束会增加（M. 沙博诺、J. M. 马林、A. 奥尔哈、R. J. 基莫夫、R. D. 利维、M. 科西奥。《胸部》106: 1695 - 1701, 1994）。本研究的目的是检验以下假设：在阻塞性吸气努力期间对上气道（UA）感觉受体的刺激有助于唤醒和呼吸暂停终止，并且随着夜间时间推移该机制的逐渐减弱会导致呼吸暂停延长。我们在连续两晚的多导睡眠图监测期间研究了7例严重阻塞性睡眠呼吸暂停患者（6名男性，1名女性）（呼吸暂停低通气指数 = 93 ± 26次/小时）。在其中一晚（随机顺序），我们用0.2%的丁卡因进行局部UA麻醉，对照夜则进行假麻醉。我们测量了呼吸暂停持续时间、呼吸暂停期间的食管压力（Pes）以及呼吸暂停时的氧饱和度下降情况。与之前的研究结果一致，对照夜从开始到结束，呼吸暂停持续时间、每次呼吸暂停的努力次数以及呼吸暂停结束时的Pes峰值均增加。UA麻醉在夜间开始时使呼吸暂停持续时间显著增加，但在夜间结束时呼吸暂停长度没有变化。麻醉夜的Pes峰值和Pes增加速率大于对照夜，但对照夜和麻醉夜开始及结束时的Pes增加速率相似。这些发现表明，UA感觉受体在夜间开始时介导呼吸暂停终止中起作用，但随着夜间时间推移这些受体的作用逐渐减弱，以至于需要更大的吸气努力来触发唤醒，从而导致呼吸暂停延长。
