Teschler H, Berthon-Jones M, Wessendorf T, Meyer H J, Konietzko N
Dept of Pneumology, Ruhrlandklinik, Medical Faculty, University of Essen, Germany.
Eur Respir J. 1996 Nov;9(11):2371-7. doi: 10.1183/09031936.96.09112371.
Snoring worsens with high alcohol consumption. It is unclear whether moderate alcohol intake worsens sleep and breathing in subjects with obstructive sleep apnoea syndrome (OSAS), and whether alcohol increases the pressure requirement for nasal continuous positive airway pressure (CPAP). Fourteen adult males with untreated OSAS but without heart or lung disease were studied (age 53+/-9 yrs, body mass index (BMI) 33+/-5 kg x m(-2) (mean+/-SD). The subjects underwent overnight polysomnography on four occasions: control, alcohol, CPAP, and alcohol + CPAP. On the alcohol nights, the subjects drank 1.5 mL x kg(-1) body weight (BW) vodka (40% alcohol by volume) (blood alcohol with and without CPAP 0.45+/-0.1 and 0.47+/-0.2 mg x mL(-1) (mean+/-SD)). On the CPAP nights, the pressure required to prevent apnoea, snoring, and silent inspiratory airflow limitation was determined using an autotitrating nasal CPAP system (ResCare AutoSet). Alcohol and control nights were performed in random order. Without CPAP, alcohol produced a small non-significant decrease in the percentage of rapid eye movement (REM) sleep (control 11+/-2 vs alcohol 8+/-1% (mean+/-SEM)), but with CPAP there was no such effect (control 15+/-2 vs 17+/-2%; CPA x alcohol interaction p=0.015). With CPAP, slow-wave sleep in the first 2 h increased slightly with alcohol (control 39+/-6 vs alcohol 51+/-4%; p=0.004). Arousal index without CPAP increased slightly with alcohol (control 43+/-5 vs alcohol 49+/-6 events x h(-1); p=0.02). There was little or no effect of alcohol on other sleep stages, arousal index, apnoea index, apnoea/hypopnoea index, mean or longest event duration, mean or worst arterial oxygen saturation, with or without CPAP, either for the full night or for the first 2 h. There was no change in the pressure requirement for CPAP (full night: control 11.9+/-0.9 vs alcohol 12.5+/-0.9 cm H2O; first 2 h: 10.9+/-0.6 vs 11.1+/-0.8 cm H2O). Moderate alcohol intake (in the form of vodka) has little effect on breathing or saturation during sleep in subjects with mild-to-severe obstructive sleep apnoea, and no effect on the pressure required for continuous positive airway pressure in order to prevent apnoea, snoring, and flow limitation. These results cannot be extrapolated to other doses or forms of alcohol, or to subjects with concurrent heart or lung disease.
饮酒量增加会使打鼾情况恶化。目前尚不清楚适度饮酒是否会使阻塞性睡眠呼吸暂停综合征（OSAS）患者的睡眠和呼吸状况恶化，以及酒精是否会增加鼻持续气道正压通气（CPAP）所需的压力。对14名未经治疗的OSAS成年男性进行了研究，但他们没有心脏病或肺部疾病（年龄53±9岁，体重指数（BMI）33±5 kg·m⁻²（平均值±标准差））。这些受试者分四次进行了整夜多导睡眠监测：对照、饮酒、CPAP以及饮酒 + CPAP。在饮酒的夜晚，受试者饮用1.5 mL·kg⁻¹体重（BW）的伏特加（体积分数为40%的酒精）（使用CPAP和未使用CPAP时的血酒精浓度分别为0.45±0.1和0.47±0.2 mg·mL⁻¹（平均值±标准差））。在使用CPAP的夜晚，使用自动调压鼻CPAP系统（ResCare AutoSet）确定预防呼吸暂停、打鼾和无声吸气气流受限所需的压力。饮酒和对照夜晚以随机顺序进行。不使用CPAP时，酒精使快速眼动（REM）睡眠百分比出现小幅但无统计学意义的下降（对照为11±2%，饮酒时为8±1%（平均值±标准误）），但使用CPAP时则没有这种影响（对照为15±2%，饮酒时为17±2%；CPAP×酒精交互作用p = 0.015）。使用CPAP时，前2小时的慢波睡眠随着饮酒略有增加（对照为39±6%，饮酒时为51±4%；p = 0.004）。不使用CPAP时，唤醒指数随着饮酒略有增加（对照为43±5次/小时，饮酒时为49±6次/小时；p = 0.02）。无论是否使用CPAP，无论是整夜还是前2小时，酒精对其他睡眠阶段、唤醒指数、呼吸暂停指数、呼吸暂停/低通气指数、平均或最长事件持续时间、平均或最差动脉血氧饱和度几乎没有或没有影响。CPAP所需压力没有变化（整夜：对照为11.9±0.9 cmH₂O，饮酒时为12.5±0.9 cmH₂O；前2小时：10.9±0.6 cmH₂O，饮酒时为11.1±0.8 cmH₂O）。适度饮酒（以伏特加形式）对轻至重度阻塞性睡眠呼吸暂停患者睡眠期间的呼吸或血氧饱和度影响很小，对预防呼吸暂停、打鼾和气流受限所需的持续气道正压通气压力没有影响。这些结果不能外推到其他剂量或形式的酒精，也不能外推到并发心脏病或肺部疾病的患者。
