title: Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension.
abstract: OBJECTIVE
  Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine.
  
  
  METHODS
  Prospective laboratory investigation using an established model of acute pulmonary hypertension.
  
  
  METHODS
  University hospital laboratory.
  
  
  METHODS
  Seven adult beagle dogs weighing 8-14 kg.
  
  
  METHODS
  After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure.
  
  
  RESULTS
  Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion.
  
  
  CONCLUSIONS
  In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.
authors.affiliation: Center for Expiremental Surgery and Anesthesiology, Anesthesiology Department, Katholieke Universiteit Leuven, Belgium.
authors.forename: H Alex
authors.initials: HA
authors.lastname: Leather
authors.forename: Patrick
authors.initials: P
authors.lastname: Segers
authors.forename: Noor
authors.initials: N
authors.lastname: Berends
authors.forename: Eugène
authors.initials: E
authors.lastname: Vandermeersch
authors.forename: Patrick F
authors.initials: PF
authors.lastname: Wouters
mesh_terms: D000208:Acute Disease; D000704:Analysis of Variance; D000818:Animals; D001127:Arginine Vasopressin / Q000009:adverse effects*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000188:drug therapy*; D010656:Phenylephrine / Q000494:pharmacology; D011446:Prospective Studies; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000009:adverse effects*; D018497:Ventricular Dysfunction, Right / Q000139:chemically induced* / Q000188:drug therapy*
chemical_list: D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin; D010656:Phenylephrine