It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia.We have investigated the relationships between pulmonary function data, sleeprelated desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O 2 therapy (daytime arterial oxygen tension (Pa,O 2 ) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending ≥30% of the recording time with a transcutaneous O 2 saturation <90%. An obstructive sleep apnoea syndrome was excluded by polysomnography.Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O 2 (8.4±0.6 vs 8.4±0.4 kPa (63±4 vs 63±3 mmHg)) but arterial carbon dioxide tension (Pa,CO 2 ) was higher in Group 1 (6.0±0.7 vs 5.3±0.5 kPa (45±5 vs 40±4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6±0.7 vs 2.5±0.6 kPa (19±5 vs 19±4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension.It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia. Is sleep-related hypoxaemia present in patients with less severe COPD with mild or absent daytime hypoxaemia? Several studies of the literature [11][12][13] have shown that a relatively high percentage of these COPD patients exhibit significant nocturnal hypoxaemia, which naturally raises the question: Does this hypoxaemia, limited to sleep, deserve treatment with nocturnal oxygen? Such a treatment could be justified if nocturnal hypoxaemia had deleterious effects on life expectancy, which is rather controversial [14,15], and on pulmonary haemodynamics. It has been hypothesized [16,17] that isolated nocturnal hypoxaemia, occurring in patients without significant daytime hypoxaemia, could lead to permanent (daytime) pulmonary hypertension, but this hypothesis has not, so...