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/minute for 30 minutes. 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 ventriculoarterial 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 mm Hg/ml, decreased end-systolic elastance from 1.11 +/- 0.07 to 0.54 +/- 0.02 mm Hg/ml, decreased 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 end-systolic elastance; however, it decreased arterial elastance to 1.84 +/- 0.33 mm Hg/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 ventriculoarterial coupling and cardiac output because of vasodilating effects.
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/minute for 30 minutes. 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 ventriculoarterial 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 mm Hg/ml, decreased end-systolic elastance from 1.11 +/- 0.07 to 0.54 +/- 0.02 mm Hg/ml, decreased 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 end-systolic elastance; however, it decreased arterial elastance to 1.84 +/- 0.33 mm Hg/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 ventriculoarterial coupling and cardiac output because of vasodilating effects.
Authors: Rebecca R Vanderpool; Ankit A Desai; Shannon M Knapp; Marc A Simon; Aiden Abidov; Jason X-J Yuan; Joe G N Garcia; Lillian M Hansen; Steven R Knoper; Robert Naeije; Franz P Rischard Journal: Eur Respir J Date: 2017-08-24 Impact factor: 16.671
Authors: Steffen Rex; Carlo Missant; Patrick Segers; Rolf Rossaint; Patrick F Wouters Journal: Intensive Care Med Date: 2007-08-21 Impact factor: 17.440