Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury

Masamitsu Sanui, David R. King, Ara J. Feinstein, Albert J. Varon, Stephen M. Conn, Kenneth G. Proctor

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

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 Design: Prospective randomized, blinded animal study. Setting: University laboratory. Subjects: Thirty-three swine. Interventions: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure ≈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·kg -1·hr -1 arginine vasopressin or placebo was titrated to a mean arterial pressure target ≥60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure ≥60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO 2 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. Measurements and Main 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 CO 2-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.

Original languageEnglish (US)
Pages (from-to)433-438
Number of pages6
JournalCritical Care Medicine
Volume34
Issue number2
DOIs
StatePublished - Feb 2006

Fingerprint

Arginine Vasopressin
Resuscitation
Hypotension
Cerebrovascular Circulation
Placebos
Shock
Carbon Monoxide
Compliance
Arterial Pressure
Intracranial Hypertension
Hemorrhagic Shock
Traumatic Brain Injury
Intracranial Pressure
Mannitol
Swine
Hemorrhage

Keywords

  • Brain tissue Po
  • Cerebral perfusion pressure
  • CO reactivity
  • Intracranial pressure
  • Shock
  • Swine

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury. / Sanui, Masamitsu; King, David R.; Feinstein, Ara J.; Varon, Albert J.; Conn, Stephen M.; Proctor, Kenneth G.

In: Critical Care Medicine, Vol. 34, No. 2, 02.2006, p. 433-438.

Research output: Contribution to journalArticle

Sanui, Masamitsu ; King, David R. ; Feinstein, Ara J. ; Varon, Albert J. ; Conn, Stephen M. ; Proctor, Kenneth G. / Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury. In: Critical Care Medicine. 2006 ; Vol. 34, No. 2. pp. 433-438.
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AU - Conn, Stephen M.

AU - Proctor, Kenneth G.

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N2 - 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 Design: Prospective randomized, blinded animal study. Setting: University laboratory. Subjects: Thirty-three swine. Interventions: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure ≈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·kg -1·hr -1 arginine vasopressin or placebo was titrated to a mean arterial pressure target ≥60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure ≥60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO 2 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. Measurements and Main 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 CO 2-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.

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