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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.

Background-Plasma levels of atrial natriuretic peptide (ANP) are elevated in patients with chronic obstructive pulmonary disease (COPD) and may have a role in preventing oedema formation in these patients. Methods-Plasma ANP levels were measured in 60 patients with COPD and these measurements were related to pulmonary haemodynamics, response to treatment during exacerbations, and clinical patterns of the stable disease. Results-Plasma ANP levels did not correlate significantly with right atrial or pulmonary arterial pressures but did correlate significantly with both the right ventricular end diastolic volume and right ventricular wall volume measured by magnetic resonance imaging. Oxygen (2 1/min by nasal prongs for 30 minutes) did not change the mean pulmonary arterial pressure or the level of plasma ANP. In 20 patients with an acute exacerbation of COPD plasma ANP levels were higher in those with oedema (302 (185) pg/ml) than in those without oedema (87 (43) pg/ml). Oxygen given for one hour had no effect on plasma levels of ANP. However, plasma ANP levels fell over the first three days during treatment in those with oedema, the fall correlating with the change in body weight. In a further 20 stable patients with hypoxic COPD, those with hypercapnia and previous episodes of oedema had higher levels of plasma ANP (120 (50) pglml) than normocapnic patients with no previous oedema (54 (15) pg/ml). Conclusions-The level of ANP is high in the plasma of patients with COPD, particularly during exacerbations in those with oedema. The association of a high plasma ANP level and volume overload is shown by the fall in ANP levels with treatment of the oedema, and the correlation between levels of ANP and right ventricular end diastolic or wall volumes. (Thorax 1993;48:730-735) The traditional view of the development of peripheral oedema in patients with chronic obstructive pulmonary disease (COPD) suggests that chronic hypoxia is responsible for pulmonary vasoconstriction which eventually leads to irreversible pulmonary hypertension, increased right ventricular work, and right ventricular failure.' 2 This sequence of events has been challenged recently.3 The right ventricular performance is relatively well preserved in patients with COPD, even in the face of pulmonary hypertension.45 Moreover, the decline in right ventricular function in patients with COPD presenting with oedema may not be as a direct result of an augmented right ventricular afterload.5 6 Furthermore, not all patients with COPD and pulmonary hypertension develop oedema, suggesting decompensated cor pulmonale during exacerbations of their condition.

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 (p < 0.01) was noted 30min 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.