title: How prostacyclin improves cardiac output in right heart failure in conjunction with pulmonary hypertension.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  We measured the effects of prostacyclin on load-independent measurements of right ventricular contractility in a model of load-induced acute right ventricular failure.
  
  
  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.affiliation: Laboratory of Physiology, Faculty of Medicine of the Free University of Brussels, Erasme Campus, CP 604, Lennik Road 808, B-1070 Brussels, Belgium.
authors.forename: Francçois
authors.initials: F
authors.lastname: Kerbaul
authors.forename: Serge
authors.initials: S
authors.lastname: Brimioulle
authors.forename: Benoît
authors.initials: B
authors.lastname: Rondelet
authors.forename: Céline
authors.initials: C
authors.lastname: Dewachter
authors.forename: Ives
authors.initials: I
authors.lastname: Hubloue
authors.forename: Robert
authors.initials: R
authors.lastname: Naeije
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects*; D004195:Disease Models, Animal; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D006976:Hypertension, Pulmonary / Q000150:complications / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000187:drug effects; D011651:Pulmonary Artery / Q000187:drug effects / Q000503:physiopathology; D014655:Vascular Resistance / Q000187:drug effects; D018497:Ventricular Dysfunction, Right / Q000150:complications / Q000503:physiopathology*
chemical_list: D000959:Antihypertensive Agents; D011464:Epoprostenol