Reduction in pulmonary hypertension by prostaglandin E1 in decompensated chronic obstructive pulmonary disease.

Prostaglandin E1 (PgE1) was administered intravenously to 26 patients with decompensated chronic obstructive pulmonary disease (COPD) in order to investigate the effects on hemodynamics and blood gases of a reduction in pulmonary hypertension in this condition. In the first 10 patients, PgE1 at 0.02 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 20 and 7%, increased cardiac index (CI) and oxygen delivery to the tissues (TO2), and did not affect blood gases. In the next 9 patients, PgE1 at 0.04 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 24 and 14%, increased CI and TO2, slightly decreased arterial oxygenation, and did not affect mixed venous blood gases. Side effects, consisting in facial flush, headache, and malaise occurred in 4 of these patients. In the last 7 patients who were artificially ventilated, PgE1 at 0.02 microgram/kg/min increased CI and TO2 but had no effect on vascular pressures and blood gases. Prostaglandin E1 was also given intravenously to 7 healthy subjects breathing 12.5% O2 in N2 for 10 min. Hypoxic pulmonary vasoconstriction was not inhibited by PgE1, even at the highest dosage of 0.04 microgram/kg/min, which caused a flush of the skin, headache, and malaise in all the subjects. Infusion of PgE1 reduces the pulmonary hypertension secondary to decompensated COPD. At adequate dosage, this effect can be obtained with minimal systemic vasodilation and no alteration in the gas exchange function of the lungs, which may be due to preservation of pulmonary vascular tone adaptation to hypoxia. The vasodilating activity fo PgE1 appears to be blunted during artificial ventilation.