OBJECT: Limited resuscitation following uncontrolled hemorrhagic shock (HS) has been associated with improved outcomes in various animal models, although it has not been previously studied in the setting of traumatic brain injury (TBI) and ethanol intoxication. The aim of the present study was to determine the effects of ethanol intoxication in a model of experimental TBI and HS treated with limited resuscitation. METHODS: After induction of anesthesia and the placement of instruments, swine were subjected to a fluid-percussion injury of 3 atm. Simultaneously, hemorrhage was induced from an arterial catheter via a computerized roller pump to a mean arterial blood pressure (MABP) of 50 mm Hg, at which time uncontrolled hemorrhage was induced by the creation of an aortic tear. When the MABP decreased to 30 mm Hg, limited resuscitation to a MABP of 60 mm Hg was begun. After 60 minutes, animals were aggressively resuscitated to baseline MABP levels. Two groups of animals were studied: those receiving tap water by gastrostomy tube and those receiving ethanol (4 g/kg) by gastrostomy tube. Animals were monitored for 180 minutes after TBI. Hemorrhage volumes were significantly greater in ethanol-infused animals (mean +/- standard deviation, 41 +/- 34 mm Hg) compared with tap water-infused animals (17 +/- 18 mm Hg; p = 0.048). Resuscitation requirements were significantly higher and metabolic parameters significantly worse in the ethanol group. Survival time was also significantly decreased in the animals infused with ethanol (81 +/- 60 minutes) compared with those infused with tap water (130 +/- 51 minutes; p = 0.035). CONCLUSIONS: Ethanol intoxication led to increased hemorrhage volume and worsened hemodynamic and metabolic profiles in this model of limited resuscitation after TBI and HS. Ethanol-exposed animals had increased resuscitation requirements and decreased survival times.
OBJECT: Limited resuscitation following uncontrolled hemorrhagic shock (HS) has been associated with improved outcomes in various animal models, although it has not been previously studied in the setting of traumatic brain injury (TBI) and ethanol intoxication. The aim of the present study was to determine the effects of ethanol intoxication in a model of experimental TBI and HS treated with limited resuscitation. METHODS: After induction of anesthesia and the placement of instruments, swine were subjected to a fluid-percussion injury of 3 atm. Simultaneously, hemorrhage was induced from an arterial catheter via a computerized roller pump to a mean arterial blood pressure (MABP) of 50 mm Hg, at which time uncontrolled hemorrhage was induced by the creation of an aortic tear. When the MABP decreased to 30 mm Hg, limited resuscitation to a MABP of 60 mm Hg was begun. After 60 minutes, animals were aggressively resuscitated to baseline MABP levels. Two groups of animals were studied: those receiving tapwater by gastrostomy tube and those receiving ethanol (4 g/kg) by gastrostomy tube. Animals were monitored for 180 minutes after TBI. Hemorrhage volumes were significantly greater in ethanol-infused animals (mean +/- standard deviation, 41 +/- 34 mm Hg) compared with tapwater-infused animals (17 +/- 18 mm Hg; p = 0.048). Resuscitation requirements were significantly higher and metabolic parameters significantly worse in the ethanol group. Survival time was also significantly decreased in the animals infused with ethanol (81 +/- 60 minutes) compared with those infused with tapwater (130 +/- 51 minutes; p = 0.035). CONCLUSIONS:Ethanol intoxication led to increased hemorrhage volume and worsened hemodynamic and metabolic profiles in this model of limited resuscitation after TBI and HS. Ethanol-exposed animals had increased resuscitation requirements and decreased survival times.
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