Badr M S, Morgan B J, Finn L, Toiber F S, Crabtree D C, Puleo D S, Skatrud J B
William S. Middleton Memorial Veterans Hospital, Department of Medicine, University of Wisconsin Medical School, Madison, USA.
Sleep. 1997 Sep;20(9):707-14. doi: 10.1093/sleep/20.9.707.
Sleep state instability is a potential mechanism of central apnea/hypopnea during non-rapid eye movement (NREM) sleep. To investigate this postulate, we induced brief arousals by delivering transient (0.5 second) auditory stimuli during stable NREM sleep in eight normal subjects. Arousal was determined according to American Sleep Disorders Association (ASDA) criteria. A total of 96 trials were conducted; 59 resulted in cortical arousal and 37 did not result in arousal. In trials associated with arousal, minute ventilation (VE) increased from 5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone breath (p = 0.001). However, no subsequent hypopnea or apnea occurred as VE decreased gradually to 4.8 +/- 1.5 l/minute (p > 0.05) on the fifth posttone breath. Trials without arousal did not result in hyperpnea on the first breath nor subsequent hypopnea. We conclude that 1) auditory stimulation resulted in transient hyperpnea only if associated with cortical arousal; 2) hypopnea or apnea did not occur following arousal-induced hyperpnea in normal subjects; 3) interaction with fluctuating chemical stimuli or upper airway resistance may be required for arousals to cause sleep-disordered breathing.
睡眠状态不稳定是非快速眼动（NREM）睡眠期间中枢性呼吸暂停/呼吸浅慢的一种潜在机制。为了研究这一假设，我们在8名正常受试者稳定的NREM睡眠期间通过给予短暂（0.5秒）听觉刺激诱导短暂觉醒。根据美国睡眠障碍协会（ASDA）标准确定觉醒。总共进行了96次试验；59次导致皮层觉醒，37次未导致觉醒。在与觉醒相关的试验中，第一次音调后呼吸时分钟通气量（VE）从5.1±1.24升/分钟增加到7.5±2.24升/分钟（p = 0.001）。然而，随后没有出现呼吸浅慢或呼吸暂停，因为在第五次音调后呼吸时VE逐渐降至4.8±1.5升/分钟（p>0.05）。无觉醒的试验在第一次呼吸时未导致呼吸急促，也未导致随后的呼吸浅慢。我们得出结论：1）听觉刺激仅在与皮层觉醒相关时才导致短暂的呼吸急促；2）正常受试者在觉醒诱导的呼吸急促后未出现呼吸浅慢或呼吸暂停；3）觉醒导致睡眠呼吸障碍可能需要与波动的化学刺激或上气道阻力相互作用。
