title: Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits.
abstract: OBJECTIVE
  Arginine vasopressin is being used increasingly to treat vasodilatory hypotension, although little is known of its effects on regional perfusion. Arginine vasopressin hemodynamic effects in physiology are mainly mediated through the V1a receptor on blood vessels. To investigate this further, we studied the effect of arginine vasopressin on systemic and renal blood flow in anesthetized, ventilated rabbits given either intravenous saline or endotoxin, and the impact of blocking V1a receptors.
  
  
  METHODS
  Prospective, randomized, controlled study.
  
  
  METHODS
  Animal research laboratory.
  
  
  METHODS
  Male White New Zealand rabbits.
  
  
  METHODS
  Measurement was made of mean arterial blood pressure, aortic and renal blood flow velocities (pulsed Doppler), and renal cortical and medullary flow (laser Doppler).
  
  
  RESULTS
  In a first series of animals, incremental intravenous boluses of arginine vasopressin ranging from 1 to 1000 ng were administered 90 mins postendotoxin or saline. In control rabbits (n = 9), increasing doses of arginine vasopressin elevated mean arterial blood pressure but reduced both aortic and renal blood flow velocity and renal cortical flow (p <.05). In endotoxic animals (n = 6), arginine vasopressin produced a similar increase in mean arterial blood pressure although aortic flow was maintained while renal blood flow velocity increased, mostly in its diastolic component (p <.05). Pretreatment with the V1a receptor antagonist in a second series of animals blunted all the effects observed in both control (n = 5) and endotoxic (n = 6) animals, suggesting that arginine vasopressin acted mainly through V1a subtype in this early phase of sepsis.
  
  
  CONCLUSIONS
  Preservation of renal blood flow with arginine vasopressin during endotoxemia, in particular to the cortex, suggests it could be a promising agent for hemodynamic support during septic shock.
authors.affiliation: Critical Care Division, Royal Victoria Hospital, Victoria, BC, Canada.
authors.forename: Martin
authors.initials: M
authors.lastname: Albert
authors.forename: Marie-Reine
authors.initials: MR
authors.lastname: Losser
authors.forename: David
authors.initials: D
authors.lastname: Hayon
authors.forename: Valérie
authors.initials: V
authors.lastname: Faivre
authors.forename: Didier
authors.initials: D
authors.lastname: Payen
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D001783:Blood Flow Velocity; D004305:Dose-Response Relationship, Drug; D006439:Hemodynamics / Q000187:drug effects*; D007672:Kidney Cortex / Q000098:blood supply / Q000187:drug effects; D007679:Kidney Medulla / Q000098:blood supply / Q000187:drug effects; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D011446:Prospective Studies; D011817:Rabbits; D011897:Random Allocation; D012044:Regression Analysis; D012079:Renal Circulation / Q000187:drug effects*; D012772:Shock, Septic / Q000188:drug therapy*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin