Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury.
OBJECTIVE
Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension.


METHODS
Prospective randomized, blinded animal study.


METHODS
University laboratory.


METHODS
Thirty-three swine.


METHODS
In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation.


RESULTS
In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin).


CONCLUSIONS
Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.
Sanui
Masamitsu
M
Department of Anesthesiology, Division of Trauma Anesthesia and Critical Care, University of Miami Miller School of Medicine, FL 33136, USA. sanui@omiya.jichi.ac.jp
King
David R
DR
Feinstein
Ara J
AJ
Varon
Albert J
AJ
Cohn
Stephen M
SM
Proctor
Kenneth G
KG
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001930:Brain Injuries / Q000150:complications*; D005440:Fluid Therapy; D007427:Intracranial Pressure / Q000187:drug effects; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000188:drug therapy / Q000209:etiology*; D013552:Swine; D014667:Vasopressins / Q000627:therapeutic use*
D014667:Vasopressins