Search

There is a complex interaction between pulmonary haemodynamics, hormonal, and salt and water balance in patients with chronic obstructive pulmonary disease (COPD) and in normal subjects exposed to hypoxia or high altitude. This study aims to investigate the effects of hypoxia on renal hormonal balance in normal subjects and patients with COPD, particularly the role of urinary dopamine and atrial natriuretic peptide (ANP). Urinary dopamine output, ANP, and plasma renin activity (PRA) were measured in 12 normal subjects exposed to hypoxia (12% O2) and hyperoxia (40% O2) for 1 h and in 15 patients with exacerbations of COPD while breathing air or O2. These measurements were repeated in six of the patients with exacerbations of COPD when they were clinically stable. Hypoxia caused an increase in ANP levels (49 +/- 6-62 +/- 6 pg ml-1, P < 0.05) and a fall in urinary dopamine output (277 +/- 39-205 +/- 33 ng h-1, P < 0.002) in normal subjects. Hyperoxia was associated with a return of plasma ANP to the baseline values. In patients with exacerbations of COPD plasma ANP levels were higher (181 +/- 36 pg ml-1) than in normal subjects (49.5 +/- 6.5 pg ml-1, P < 0.001). Urinary dopamine output breathing air (175 +/- 34 ng h-1) was similar to the levels when normal subjects were made hypoxaemic and PRA was elevated in comparison to normal values. There was no change in their levels following the acute administration of oxygen in patients presenting with exacerbations of COPD, but oxygen improved urinary sodium excretion (P < 0.05). In six patients re-studied when clinically stable there was a fall in urinary dopamine output, plasma ANP and PRA when breathing air in comparison to the acute stage of the disease (P < 0.05). These data suggest presence of renal hormonal imbalance including endogenous urinary dopamine output during hypoxic exacerbation of COPD and in normal subjects exposed to hypoxia.

We have studied the effects of ibopamine, an oral dopamine derivative, on pulmonary hemodynamics and blood gas values when given as a single oral dose (100 mg) to patients with severe hypoxic chronic obstructive pulmonary disease. A small but significant increase in mean pulmonary arterial pressure from 29 +/- 8 to 32 +/- 7 mm Hg (p0.01) was noted 30 min after ibopamine was given associated with a small increase in cardiac index. No other consistent hemodynamic changes were observed, and no alteration in blood gas values or oxygen saturation occurred. These results do not indicate a role for ibopamine in the treatment of patients with hypoxic chronic obstructive pulmonary disease and pulmonary hypertension, but, in addition, do not indicate any major deleterious effects of ibopamine on pulmonary hemodynamics or blood gas values in such patients.