title: Impact of vasopressin on hemodynamic and metabolic function in the decompensatory phase of hemorrhagic shock.
abstract: OBJECTIVE
  To explore how the potent vasoconstrictive features of vasopressin impact the rate of cardiovascular collapse and metabolic derangements associated with prolonged hemorrhagic shock.
  
  
  METHODS
  A prospective randomized trial.
  
  
  METHODS
  University hospital-based animal laboratory.
  
  
  METHODS
  Sixteen swine.
  
  
  METHODS
  Swine were bled in an isobaric fashion to achieve a linear decrease in the mean arterial blood pressure to 40 mmHg. The mean arterial blood pressure was then maintained at 40 mmHg until the onset of cardiovascular decompensation, defined as the need to reinfuse shed blood to maintain the blood pressure at 40 mmHg. Once at the onset of cardiovascular decompensation, animals were randomly assigned to 2 resuscitation groups: the crystalloid group received lactated Ringer's solution and the vasopressin group received lactated Ringer's solution and arginine vasopressin. Resuscitation consisted of infusing lactated Ringer's solution with and without vasopressin (0.05 U/kg/min) to maintain a blood pressure of 70 mmHg for 60 minutes.
  
  
  RESULTS
  The rate of crystalloid infusion was compared between groups using an unpaired 2-tailed t test. Metabolic and hemodynamic parameters between groups over time were compared with a repeated measures analysis of variance. Vasopressin decreased the rate of crystalloid infusion during resuscitation by 50%. During resuscitation, the cardiac index in the crystalloid group was restored to near baseline levels and was decreased to near half of baseline levels in the vasopressin group. Animals in the vasopressin group developed a lactic acidemia, but animals in the crystalloid group revealed no change from baseline in the arterial pH and a slight decrease in the plasma lactate.
  
  
  CONCLUSIONS
  Administration of vasopressin used as an adjunct to maintain blood pressure in the decompensatory phase of hemorrhagic shock slows cardiovascular collapse, but has an adverse effect on metabolic and hemodynamic function. Further investigation is warranted to clarify the role of vasopressin in the delayed management of severe hemorrhagic shock.
authors.affiliation: Department of Anesthesiology, University of Utah School of Medicine, Salt Lake City, UT 84132-2304, USA. Ken.B.Johnson@hsc.utah.edu
authors.forename: Ken B
authors.initials: KB
authors.lastname: Johnson
authors.forename: Frederick J
authors.initials: FJ
authors.lastname: Pearce
authors.forename: Nicole
authors.initials: N
authors.lastname: Jeffreys
authors.forename: Scott W
authors.initials: SW
authors.lastname: McJames
authors.forename: Mark
authors.initials: M
authors.lastname: Cluff
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D004195:Disease Models, Animal; D005260:Female; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000097:blood*; D008297:Male; D012771:Shock, Hemorrhagic / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D013552:Swine; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014667:Vasopressins / Q000627:therapeutic use*
chemical_list: D014662:Vasoconstrictor Agents; D014667:Vasopressins; D019344:Lactic Acid