Dawson A, Bigby B G, Poceta J S, Mitler M M
Division of Sleep Disorders, Scripps Clinic and Research Foundation, La Jolla, California 92037, USA.
Alcohol Clin Exp Res. 1997 Apr;21(2):183-90.
We measured inspiratory resistance (R1), inspiratory occlusion pressure (P0.1), and the ventilatory responses to hypercapnia and isocapnic hypoxia during waking and during stage 2 non-rapid eye movement sleep in nine young men who were habitual snorers. They were studied on 2 nights during the 3 hours after receiving a bedtime drink containing either a placebo or 100-proof vodka (1.5 ml/kg) in orange juice. We compared the results with those we reported previously in 10 nonsnoring but otherwise similar men. Waking R1 was the same in nonsnorers and snorers, and it was not affected by ethanol. During sleep on the control night, R1 increased by 70% in nonsnorers and by 280% in snorers. On the ethanol night, the increase from waking to sleeping was more than doubled in both nonsnorers and snorers. P0.1 and the responses to hypercapnia and hypoxia showed no differences between nonsnorers and snorers, therefore the results from the two groups were pooled. Minute ventilation and the hypercapnic response decreased from waking to sleeping and P0.1 was more negative during sleep, but there was no significant effect of ethanol. There was a significant correlation between the changes from waking to sleeping in R1 and P0.1 on the ethanol night suggesting that inspiratory effort increased in response to the increased resistance. The response to isocapnic hypoxia showed no effect of either sleep state or drink. Inspiratory time did not change but mean inspiratory flow (VT/T1) was significantly reduced during sleep on both control and ethanol nights. The duty cycle ratio (T1/Ttot) was significantly increased during sleep on the ethanol night. Despite its great effect on inspiratory resistance, especially in snorers, ethanol, in the dose used in our study, does not augment the depression of minute ventilation or of the hypercapnic response that occur normally in stage 2 non-rapid eye movement sleep. After ethanol, our subjects showed the decreased VT/T1 and the increased T1/Ttot that occur normally during sleep in response to an inspiratory resistive load. However, they also showed increased inspiratory effort. The combination of increased inspiratory resistance and greater inspiratory effort would increase the tendency of an unstable upper airway to collapse and could account for the aggravation of obstructive sleep apnea by ethanol.
我们测量了9名习惯性打鼾的年轻男性在清醒状态和非快速眼动睡眠2期时的吸气阻力（R1）、吸气阻断压（P0.1）以及对高碳酸血症和等碳酸血症性低氧的通气反应。在两个晚上，睡前给他们喝一杯含有安慰剂或100度伏特加（1.5毫升/千克）的橙汁饮料，3小时后对他们进行研究。我们将结果与之前报道的10名不打鼾但其他方面相似的男性的结果进行了比较。清醒时，非打鼾者和打鼾者的R1相同，且不受乙醇影响。在对照夜睡眠期间，非打鼾者的R1增加了70%，打鼾者增加了280%。在乙醇夜，非打鼾者和打鼾者从清醒到睡眠时R1的增加都增加了一倍多。P0.1以及对高碳酸血症和低氧的反应在非打鼾者和打鼾者之间没有差异，因此将两组结果合并。分钟通气量和高碳酸血症反应从清醒到睡眠时降低，睡眠时P0.1更负，但乙醇没有显著影响。在乙醇夜，从清醒到睡眠时R1和P0.1的变化之间存在显著相关性，表明吸气努力随着阻力增加而增加。对等碳酸血症性低氧的反应不受睡眠状态或饮料的影响。吸气时间没有变化，但在对照夜和乙醇夜睡眠期间，平均吸气流量（VT/T1）显著降低。乙醇夜睡眠期间，占空比（T1/Ttot）显著增加。尽管乙醇对吸气阻力有很大影响，尤其是对打鼾者，但在我们研究中使用的剂量下，乙醇不会增强在非快速眼动睡眠2期通常发生的分钟通气量或高碳酸血症反应的抑制。摄入乙醇后，我们的受试者出现了睡眠期间正常出现的VT/T1降低和T1/Ttot增加，这是对吸气阻力负荷的反应。然而，他们也表现出吸气努力增加。吸气阻力增加和吸气努力增强相结合会增加不稳定的上气道塌陷的倾向，这可能解释了乙醇会加重阻塞性睡眠呼吸暂停。
