Amatoury Jason, Azarbarzin Ali, Younes Magdy, Jordan Amy S, Wellman Andrew, Eckert Danny J
Neuroscience Research Australia (NeuRA), and the School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Sleep. 2016 Dec 1;39(12):2091-2100. doi: 10.5665/sleep.6304.
Arousals from sleep vary in duration and intensity. Accordingly, the physiological consequences of different types of arousals may also vary. Factors that influence arousal intensity are only partly understood. This study aimed to determine if arousal intensity is mediated by the strength of the preceding respiratory stimulus, and investigate other factors mediating arousal intensity and its role on post-arousal ventilatory and pharyngeal muscle responses.
Data were acquired in 71 adults (17 controls, 54 obstructive sleep apnea patients) instrumented with polysomnography equipment plus genioglossus and tensor palatini electromyography (EMG), a nasal mask and pneumotachograph, and an epiglottic pressure sensor. Transient reductions in CPAP were delivered during sleep to induce respiratory-related arousals. Arousal intensity was measured using a validated 10-point scale.
Average arousal intensity was not related to the magnitude of the preceding respiratory stimuli but was positively associated with arousal duration, time to arousal, rate of change in epiglottic pressure and negatively with BMI (R > 0.10, P ≤ 0.006). High (> 5) intensity arousals caused greater ventilatory responses than low (≤ 5) intensity arousals (10.9 [6.8-14.5] vs. 7.8 [4.7-12.9] L/min; P = 0.036) and greater increases in tensor palatini EMG (10 [3-17] vs. 6 [2-11]%max; P = 0.031), with less pronounced increases in genioglossus EMG.
Average arousal intensity is independent of the preceding respiratory stimulus. This is consistent with arousal intensity being a distinct trait. Respiratory and pharyngeal muscle responses increase with arousal intensity. Thus, patients with higher arousal intensities may be more prone to respiratory control instability. These findings are important for sleep apnea pathogenesis.
睡眠中的觉醒在持续时间和强度上存在差异。因此,不同类型觉醒的生理后果也可能不同。影响觉醒强度的因素仅得到部分理解。本研究旨在确定觉醒强度是否由先前呼吸刺激的强度介导,并研究介导觉醒强度的其他因素及其对觉醒后通气和咽肌反应的作用。
对71名成年人(17名对照者,54名阻塞性睡眠呼吸暂停患者)进行数据采集,这些人配备了多导睡眠图设备以及颏舌肌和腭帆张肌肌电图(EMG)、鼻面罩、呼吸流速仪和会厌压力传感器。在睡眠期间给予持续气道正压通气(CPAP)的短暂降低以诱发与呼吸相关的觉醒。使用经过验证的10分制量表测量觉醒强度。
平均觉醒强度与先前呼吸刺激的幅度无关,但与觉醒持续时间、觉醒时间、会厌压力变化率呈正相关,与体重指数呈负相关(R>0.10,P≤0.006)。高强度(>5)觉醒比低强度(≤5)觉醒引起更大的通气反应(10.9[6.8 - 14.5]对7.8[4.7 - 12.9]升/分钟;P = 0.036)和腭帆张肌EMG更大的增加(10[3 - 17]对6[2 - 11]%最大值;P = 0.031),而颏舌肌EMG的增加不太明显。
平均觉醒强度与先前的呼吸刺激无关。这与觉醒强度是一种独特特征一致。呼吸和咽肌反应随觉醒强度增加。因此,觉醒强度较高的患者可能更容易出现呼吸控制不稳定。这些发现对睡眠呼吸暂停的发病机制很重要。