Hlavac Michael C, Catcheside Peter G, McDonald Rachel, Eckert Danny J, Windler Samantha, McEvoy R Doug
Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia, Australia.
Sleep. 2006 May;29(5):624-31.
Sustained hypoxia is a neurocognitive depressant, which has been shown to impair respiratory load sensation. Hypoxia has also been shown to impair arousal in animal models, but the effects of sustained hypoxia on arousal in humans have not been studied. The aim of this study was to assess the effects of sustained hypoxia on arousal from sleep in normal subjects.
Twelve normal male subjects (age, 24.3 +/- 1.2 years; body mass index, 24.8 +/- 1.4 kg/m2) were studied during stable stage 2 non-rapid eye movement sleep on 2 separate nights 1 week apart.
Sleep physiology laboratory.
Normal healthy volunteers.
Arousal responses to external resistive loads (18 cm H2O x L(-1) x sec(-1)) and occlusions were compared during room-air breathing following sustained normoxia and isocapnic hypoxia (SaO2 approximately 85%).
Time to arousal and minimum esophageal pressure preceding arousal were measured. Time to arousal was significantly increased following hypoxia compared with normoxia for resistive loads (24.6 + 4.4 seconds vs. 12.6 +/- 1.9 seconds, p = .007) but not occlusions. Minimum esophageal pressure prior to arousal was more negative following hypoxia for both external loads (-16.8 +/- 1.2 vs. -13.5 +/- 1.3 cm H2O, p = .035) and occlusions (-19.6 +/- 2.2 vs. -15.1 +/- 1.5 cm H2O, p = .029).
We conclude that sustained isocapnic hypoxia delays arousal to inspiratory loading during sleep and increases the respiratory arousal threshold. This has implications for disorders characterized by sustained nocturnal hypoxia, such as neuromuscular weakness, chronic obstructive pulmonary disease, obesity-hypoventilation syndrome, and severe obstructive sleep apnea.
持续性低氧是一种神经认知抑制剂，已被证明会损害呼吸负荷感知。低氧在动物模型中也被证明会损害觉醒，但持续性低氧对人类觉醒的影响尚未得到研究。本研究的目的是评估持续性低氧对正常受试者睡眠中觉醒的影响。
选取12名正常男性受试者（年龄24.3±1.2岁；体重指数24.8±1.4kg/m²），在间隔1周的2个不同夜晚的稳定2期非快速眼动睡眠期间进行研究。
睡眠生理学实验室。
正常健康志愿者。
在持续常氧和等碳酸血症性低氧（动脉血氧饱和度约85%）后，比较在室内空气呼吸期间对外部阻力负荷（18cmH₂O×L⁻¹×sec⁻¹）和阻塞的觉醒反应。
测量觉醒时间和觉醒前的最低食管压力。与常氧相比，低氧后对阻力负荷的觉醒时间显著延长（24.6 + 4.4秒对12.6±1.9秒，p = 0.007），但对阻塞的觉醒时间没有显著变化。对于两种外部负荷，低氧后觉醒前的最低食管压力更负（-16.8±1.2对-13.5±1.3cmH₂O，p = 0.035），对阻塞也是如此（-19.6±2.2对-15.1±1.5cmH₂O，p = 0.029）。
我们得出结论，持续性等碳酸血症性低氧会延迟睡眠期间对吸气负荷的觉醒，并增加呼吸觉醒阈值。这对以持续性夜间低氧为特征的疾病有影响，如神经肌肉无力、慢性阻塞性肺疾病、肥胖低通气综合征和严重阻塞性睡眠呼吸暂停。
