Published ahead of print on February 1, 2007, doi:10.1164/rccm.200611-1615OC
© 2007 American Thoracic Society doi: 10.1164/rccm.200611-1615OC
How Prostacyclin Improves Cardiac Output in Right Heart Failure in Conjunction with Pulmonary Hypertension1 Laboratory of Physiology, Faculty of Medicine of the Free University of Brussels, Brussels, Belgium; and 2 Department of Intensive Care, Erasme University Hospital, Brussels, Belgium Correspondence and requests for reprints should be addressed to Dr. R. Naeije, M.D., Ph.D. Department of Physiology, Faculty of Medicine of the Free University of Brussels, Erasme Campus, CP 604, Lennik Road 808, B-1070 Brussels, Belgium. E-mail: rnaeije{at}ulb.ac.be 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.
Key Words: right heart failure • contractility • heart failure • pulmonary hypertension • prostaglandins
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
