The hemodynamic effect of prostaglandin F2 alpha (PGF2 alpha) and of prostaglandin E2 (PGE2) was studied in 12 healthy volunteers admitted for suction abortion at 10--12 weeks of gestation. They were anesthesized using natrium thiomebumal, pethidine and pancuronium bromide. PGF 2 alpha was given as an intravenous infusion of 100 micrograms/min, the dose being increased by 100 micrograms every 10 min to a maximum of 300 micrograms/min. PGE2 was administered with 5 micrograms/min, the dose being increased by 5 micrograms every 10 min to a maximum of 15 micrograms/min. During infusion of 300 micrograms PGF2 alpha a significant increase iun cardiac output and femoral arterial pressure of 40% and 25% respectively was measured together with an increase in the pulmonary arterial pressure (125%). Pulmonary vascular resistance was doubled, with a concomitant decrease in systemic resistance (11%). These changes were followed by a significant decrease in pH and PaO2, whereas an increase in PaCO2 was found. During infusion of PGE2 a significant, 36% increase in cardiac output was measured during infusion of 15 micrograms/min PGE2, together with a decrease in systemic blood pressure (31%) and resistance (33%). Heart rate rose significantly, while stroke volume showed only a small increase, and pulmonary pressure was unchanged. These changes were followed by an increase in PaO2. PGF2 alpha seems to have a positive inotropic effect on the heart, whereas its response to PGE2 seems to be a result of the peripheral vasodilatation. The slight decrease in systemic blood pressure without change in pulmonary hemodynamics makes PGE2 suitable for induction in patients with cardiopulmonary diseases.