SUMMARY To evaluate the effects of prostacyclin (prostaglandin 12) 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 1/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.PRIMARY pulmonary hypertension (PPH) is characterized by extreme elevations in pulmonary vascular resistance, which ultimately result in right ventricular failure and death. The cause of this disease is unknown, but prolonged vasoconstriction has been suggested as an etiologic factor.1-' Recent studies demonstrating that vasodilators such as isoproterenol,45 hydralazine,6 and diazoxide7 I can reduce pulmonary vascular resistance in PPH provide further evidence that active pulmonary vasoconstriction may be present and potentially reversible in some patients.Prostacyclin (PGI2), a metabolite of arachidonic acid, is produced in vascular endothelial cells.9-10 Intravenous prostacyclin causes pulmonary vasodilation in animals when pulmonary vascular tone is enhanced either by hypoxiall 12 or by the infusion of ADP.'3 Prostacyclin reportedly reduced pulmonary vascular resistance in a patient with persistent fetal circulation'4 and in a patient with PPH, 15 and endogenous prostacyclin may be responsible for the reduction in pulmonary vascular tone produced by hydralazine.'6 Since intrapulmonary platelet aggregation, as a result of the reduced pulmonary blood flow, could further compromise the pulmonary circulation in PPH, the potent pulmonary vasodilator and the antiplatelet aggregatory actions of prostacyclin'°could be beneficial in this disease. We therefore evaluated the hemodynamic effects of i. v. prostacyclin in seven patients with PPH. Methods SubjectsSeven patients with PPH entered the study after giving informed consent. All seven patients had symptoms of fatigue and exertional dyspnea, and four had had syncopal episodes. The diagnosis of PPH was made after pulmonary function studies, ventilationperfusion lung scans and cardiac catheterization revealed no evidence of other causes for pulmonary arterial hypertension. Six of the seven patients underwent pulmonary ateriography, which showed no evidence of thromboembolic disease. Echocardiography was performed on all seven ...

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