title: The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo.
abstract: OBJECTIVE
  The principal effects of prostaglandin I(2) are vasodilation and inhibition of platelet aggregation induced by a rise in the intracellular second messenger cAMP. In the heart a rise in intracellular myocardial cAMP increases contractility. We examined whether prostaglandin I(2) increases left ventricular contractility in vivo. The effects of epoprostenol and iloprost on left ventricular contractility were assessed in vivo and compared to the effects of adenosine and sodium nitroprusside, which exerts vasodilatory properties independently of cAMP.
  
  
  METHODS
  Prospective, randomized, cross-over in a university laboratory.
  
  
  METHODS
  Eleven pigs (25.9+/-2.8 kg, balanced anesthesia).
  
  
  METHODS
  Each animal was exposed to intravenous sodium nitroprusside, adenosine, and epoprostenol in randomized order. Iloprost was administered at the end due to its longer half-life. The dose was titrated to achieve a 25% reduction in diastolic aortic pressure.
  
  
  RESULTS
  Left ventricular contractility was assessed before, during, and after each intervention by determination of the endsystolic elastance with the conductance method. While there was no change in endsystolic elastance upon the infusion of adenosine and sodium nitroprusside; endsystolic elastance increased in the case of epoprostenol (57%) and iloprost (71%).
  
  
  CONCLUSIONS
  Left ventricular contractility is increased in vivo by epoprostenol and iloprost but not by adenosine or sodium nitroprusside at equipotent hypotensive dose. A contribution of sympathetic reflex activation of cardiac nerves on the increase in left ventricular contractility cannot be completely ruled out.
authors.affiliation: Clinic of Anesthesiology, Ludwig Maximilian University, Klinikum Grosshadern, Marchioninistrasse 15, 81377 Munich, Germany.
authors.forename: Hille
authors.initials: H
authors.lastname: Kisch-Wedel
authors.forename: Gregor
authors.initials: G
authors.lastname: Kemming
authors.forename: Franz
authors.initials: F
authors.lastname: Meisner
authors.forename: Michael
authors.initials: M
authors.lastname: Flondor
authors.forename: Wolfgang M
authors.initials: WM
authors.lastname: Kuebler
authors.forename: Sebastian
authors.initials: S
authors.lastname: Bruhn
authors.forename: Carolina
authors.initials: C
authors.lastname: Koehler
authors.forename: Bernhard
authors.initials: B
authors.lastname: Zwissler
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D011464:Epoprostenol / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects; D007022:Hypotension / Q000139:chemically induced; D016285:Iloprost / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects*; D009599:Nitroprusside / Q000494:pharmacology; D011897:Random Allocation; D013318:Stroke Volume / Q000187:drug effects; D013552:Swine; D014665:Vasodilator Agents / Q000494:pharmacology*; D016277:Ventricular Function, Left / Q000187:drug effects*; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D011464:Epoprostenol; D016285:Iloprost; D000241:Adenosine