Acute effects of oral captopril on hemodynamics in patients with cor pulmonale

The cause of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) is considered to be hypoxic pulmonary vasoconstriction, which may be mediated in part by angiotensin II. We administered captopril (25 mg, orally) to seven patients with COPD and complicating cor pulmonale in stable state. Hemodynamic responses were recorded before and one hour after the administration of the drug. Captopril increased cardiac output by 23% (p less than 0.025) and reduced mean systemic pressure by 12% (p less than 0.004), but did not alter mean pulmonary arterial pressure. Pulmonary and systemic vascular resistance fell, respectively, by 14% (p less than 0.035) and 31% (p less than 0.03). There was an increase in pulmonary/systemic vascular resistance ratio (p less than 0.007). Heart rate, mean right atrial, pulmonary capillary wedge pressure, arterial oxygen tension and dioxide tension, and alveolar- arterial oxygen tension difference remained unchanged. These results suggest that captopril is successful in reducing pulmonary vascular resistance without affecting arterial blood gases, but does not change mean pulmonary arterial pressure probably because of the concurrent increase in pulmonary blood flow. In addition, results indicate that captopril has more effects on the systemic vasculature than on the pulmonary circulation.