Rationale. Prostacyclin therapy improves patients with pulmonary arterial hypertension, but whether this is attributable to an improved inotropic state of the right ventricle in addition to a decreased pulmonary arterial pulmonary vascular resistance remains unclear. Objectives. We measured the effects of prostacyclin on load-independent measurements of right ventricular contractility in a model of load-induced acute right ventricular failure. Methods and results. Persistent right ventricular failure was induced in dogs by a transient (90 min) pulmonary arterial constriction. After constriction release and stabilization, intravenous prostacyclin (epoprostenol) was given at doses of 6 and 12 ng/kg/min for 30 min. Pulmonary vascular resistance was assessed by pressure-flow relationships and right ventricular afterload by effective pulmonary arterial elastance. Right ventricular contractility was estimated by end-systolic elastance and right ventriculo-arterial coupling efficiency by the ratio of these elastances. Transient pulmonary arterial constriction persistently increased pulmonary vascular resistance, increased arterial elastance from 1.00 ± 0.07 to 2.86 ± 0.26 mmHg/ml, decreased end-systolic elastance from 1.11 ±0.07 to 0.54 ± 0.02 mmHg/ml, the ratio of elastances from 1.14 ± 0.08 to 0.20 ± 0.02, and cardiac output from 4.6 ± 0.1 to 2.3 ±0.1 L/min (P < 0.05). Epoprostenol did not affect endsystolic elastance, decreased arterial elastance Ea to 1.84 ± 0.33 mmHg/ml, and increased the ratio of elastances to 0.46 ± 0.17 and cardiac output to 3.4 ± 0.3 L/min (P < 0.05). Conclusions. In this model of afterload-induced right ventricular failure, prostacyclin improves right ventriculo-arterial coupling and cardiac output because of vasodilating effects.