Brander P E, Kuitunen T, Salmi T, Partinen M
Dept of Pulmonary Medicine, Helsinki University, Finland.
Eur Respir J. 1992 Mar;5(3):308-12.
The effect of a moderate oral dose of ethanol/(0.5 g.kg-1 body weight) on nocturnal arterial oxygen saturation (SaO2) was evaluated in nine male patients with advanced chronic obstructive pulmonary disease (COPD), (median forced expiratory volume in one second (FEV1) 0.9 l, arterial oxygen tension (PaO2) 9.3 kPa, arterial carbon dioxide tension (PaCO2) 5.3 kPa). During the four study nights (two after alcohol and two after placebo intake), the patients were monitored by whole-night computerized recordings of SaO2 (Biox-oximeter), airflow (thermistors) and respiratory as well as body movements (static charge sensitive bed). After alcohol intake, the mean blood ethanol concentration (SEM) in the evening was 42(2.3) mg.100 ml-1. Alcohol intake was associated with a marginal deterioration of nocturnal oxygenation; the mean (SEM) nocturnal SaO2 was 88.4(2.0) % after alcohol ingestion and 89.1(1.6) % after placebo ingestion, respectively. Only during the first 2 h in bed was there a statistically significant difference in SaO2 in favour of placebo (p less than 0.05). It is concluded that moderate alcohol intake in the evening, corresponding to "social" drinking, did not substantially aggravate nocturnal oxygenation in our patients with advanced COPD and mild to moderate daytime hypoxaemia.
对9例晚期慢性阻塞性肺疾病（COPD）男性患者（一秒用力呼气量（FEV1）中位数为0.9升，动脉血氧分压（PaO2）为9.3 kPa，动脉血二氧化碳分压（PaCO2）为5.3 kPa）评估了口服中等剂量乙醇（0.5 g·kg-1体重）对夜间动脉血氧饱和度（SaO2）的影响。在四个研究夜间（两个在饮酒后，两个在服用安慰剂后），通过对SaO2（Biox血氧计）、气流（热敏电阻）以及呼吸和身体运动（静电荷敏感床）进行整夜计算机记录来监测患者。饮酒后，晚上的平均血液乙醇浓度（标准误）为42（2.3）mg·100 ml-1。饮酒与夜间氧合略有恶化相关；饮酒后夜间SaO2的平均值（标准误）为88.4（2.0）%，服用安慰剂后为89.1（1.6）%。仅在卧床的前2小时，SaO2在统计学上有显著差异，有利于安慰剂组（p<0.05）。结论是，在我们这些晚期COPD且白天有轻度至中度低氧血症的患者中，对应于“社交”饮酒量的晚上适度饮酒，并未显著加重夜间氧合。
