Prostacyclin-induced acute pulmonary vasodilation in primary pulmonary hypertension

Abstract

To evaluate the effects of prostacyclin (prostaglandin I2) on pulmonary vascular tone in primary pulmonary hypertension (PPH), we performed right-heart catheterization on seven patients with PPH and made hemodynamic measurements before and after infusing incremental doses of prostacyclin. In maximal doses of 2-12 ng/kg/min (mean 5.7 ± 3.1 ng/kg/min), prostacyclin reduced mean pulmonary arterial pressure from 62 ± 15 to 55 ± 16 mm Hg (p < 0.05) and total pulmonary resistance from 17.1 ± 8.7 to 9.7 ± 5.9 units (p < 0.005), and increased cardiac output from 4.22 ± 1.64 to 6.57 ± 2.04 l/min (p < 0.01). Heart rate increased from 83 ± 13 to 94 ± 11 beats/min (p = 0.1) and mean systemic arterial pressure decreased from 90 ± 12 to 77 ± 4 mm Hg (p = 0.055). Three patients who received a continuous infusion of prostacyclin for 24-48 hours had sustained reductions in total pulmonary resistance during the infusion period. These data demonstrate that prostacyclin can increase cardiac output and reduce pulmonary arterial pressure and resistance in PPH.