McNicholas W T, Tarlo S, Cole P, Zamel N, Rutherford R, Griffin D, Phillipson E A
Am Rev Respir Dis. 1982 Oct;126(4):625-8. doi: 10.1164/arrd.1982.126.4.625.
The possible role of high nasal airway resistance in the pathogenesis of obstructive sleep apnea has been examined in 7 patients with seasonal (ragweed) allergic rhinitis, a naturally occurring model of reversible nasal obstruction. Measurements of nasal resistance and overnight polysomnographic studies were performed during the ragweed season when the patients complained of nasal obstruction; and 6 to 8 wk later when the symptoms had subsided (control study). During the symptomatic phase, mean (+/- SE) nasal resistance was 4.9 +/- 0.8 cm H2O/L/s, and the patients experienced 1.7 +/- 0.3 obstructive apneas per hour of sleep. In contrast, at the time of the control study, nasal resistance had decreased to 2.5 +/- 0.3 cm H2O/L/s (p less than 0.01); and the rate of obstructive apneas had decreased to 0.7 +/- 0.4 per hour of sleep (p less than 0.005). The duration of these apneas had also decreased from 15.5 +/- 0.8 s to 6.1 +/- 2.9 s (p less than 0.01). Apneas were rarely associated with significant O2 desaturation and were fewer in number than typically seen in a clinically significant sleep apnea syndrome. In male patients there was a direct relationship (r = 0.9) between the change in nasal resistance from symptomatic to control studies and the corresponding change in frequency of obstructive sleep apneas. Coincident with these respiratory changes at the time of the control study was an increase in the amount of slow-wave sleep (p = 0.05) and a small reduction in the frequency of arousals during sleep (p = NS). We conclude that in patients with allergic rhinitis, obstructive sleep apneas are longer and more frequent during a period of symptomatic nasal obstruction than when symptoms are absent. The results support the concept that a high nasal resistance may be a contributing factor in the pathogenesis of obstructive sleep apneas in general.
高鼻气道阻力在阻塞性睡眠呼吸暂停发病机制中的可能作用，已在7例季节性（豚草）过敏性鼻炎患者中进行了研究，这是一种自然发生的可逆性鼻阻塞模型。在豚草季节，当患者主诉鼻阻塞时，进行鼻阻力测量和整夜多导睡眠图研究；6至8周后，当症状消退时，进行对照研究。在症状期，平均（±标准误）鼻阻力为4.9±0.8 cmH₂O/L/s，患者每小时睡眠中出现1.7±0.3次阻塞性呼吸暂停。相比之下，在对照研究时，鼻阻力已降至2.5±0.3 cmH₂O/L/s（p<0.01）；阻塞性呼吸暂停发生率已降至每小时睡眠0.7±0.4次（p<0.005）。这些呼吸暂停的持续时间也从15.5±0.8秒降至6.1±2.9秒（p<0.01）。呼吸暂停很少与显著的氧饱和度降低相关，且数量比临床上显著的睡眠呼吸暂停综合征中通常所见的要少。在男性患者中，从症状期到对照研究期间鼻阻力的变化与阻塞性睡眠呼吸暂停频率的相应变化之间存在直接关系（r = 0.9）。对照研究时，与这些呼吸变化同时出现的是慢波睡眠量增加（p = 0.05），睡眠中觉醒频率略有降低（p = 无统计学意义）。我们得出结论，在过敏性鼻炎患者中，有症状的鼻阻塞期比无症状时，阻塞性睡眠呼吸暂停更长且更频繁。结果支持这样的概念，即高鼻阻力可能是一般阻塞性睡眠呼吸暂停发病机制中的一个促成因素。
