Objectives: Ethanol intoxication has hemodynamic and metabolic effects after hemorrhage according to studies using fixed-volume controlled blood loss models. The authors tested the null hypothesis that after uncontrolled hemorrhage there would be no difference in the hemodynamic responses between ethanol-intoxicated (EtOH+) and nonintoxicated (EtOH-) rats.
Methods: Forty Sprague-Dawley rats were anesthetized with althesin intraperitoneally. Twenty EtOH+ rats received a 3-g/kg dose of 20% ethanol intraperitoneally 60 minutes before hemorrhage. The EtOH- rats received an equivalent volume of normal saline intraperitoneally. The femoral artery was cannulated by cutdown to monitor the mean arterial blood pressure (MAP) and to obtain blood samples for lactate (LAC). Twenty rats (ten EtOH+ and ten EtOH-) underwent uncontrolled hemorrhage by 75% tail amputation. Twenty rats (ten EtOH+ and ten EtOH-) served as nonhemorrhage controls. The MAP, LAC, and cumulative hemorrhage volume were measured prehemorrhage and then every 15 minutes posthemorrhage for 120 minutes. Data were reported as mean +/- SEM. Group comparisons were analyzed by analysis of variance with repeated values and post hoc testing by Bonferroni (two tailed; alpha = 0.05).
Results: Initially, EtOH+ and EtOH- rats were evenly matched for LAC and MAP. The mean (+/-SD) baseline ethanol level was 170 (+/-68) mg/dL in EtOH+ rats. Cumulative hemorrhage volume was similar (p = 0.23) for the EtOH- (2.36 +/- 0.24 mL/100 g) and EtOH+ (1.87 +/- 0.32 mL/100 g) rats. No significant difference was noted in posthemorrhage MAP between EtOH- (68.6 +/- 6.8 mm Hg) and EtOH+ (69.3 +/- 7.2 mm Hg) rats (p = 1.00). The EtOH- group had a significantly higher LAC (4.94 +/- 1.07 mmol/L) than the EtOH+ group (2.27 +/- 0.59 mmol/L) (p < 0.03).
Conclusions: Ethanol intoxication does not deleteriously affect the hemodynamic response to uncontrolled hemorrhage.