The effect of ethanol intoxication on the response to uncontrolled hemorrhage in a rodent model

Study objectives: Ethanol intoxication has been shown to have significant hemodynamic and metabolic effects after hemorrhage, according to studies using fixed-volume controlled blood loss models. We present an acute ethanol-intoxicated uncontrolled hemorrhage model in which we tested the null hypothesis that there would be no difference in the hemorrhage volumes and hemodynamic responses between ethanol intoxicated (EtOH+) rats and nonintoxicated (EtOH–) rats. Methods: Forty Sprague-Dawley rats were anesthetized with Althesin by the intraperitoneal route (IP). Twenty (EtOH+) rats received a 3 g/kg dose of 20% ethanol (IP) 60 minutes before uncontrolled hemorrhage. The ETOH– rats received an equivalent volume of normal saline solution IP. The femoral artery was cannulated by cutdown to monitor the mean arterial blood pressure (MAP) and to obtain blood samples for lactate. Twenty (10 EtOH+, 10 EtOH–) rats underwent uncontrolled hemorrhage by 75% tail amputation. Twenty (10 EtOH+, 10 EtOH–) rats served as nonhemorrhage controls. The MAP, lactate, and cumulative hemorrhage volume per 100 g of rat weight (CHV) 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; post hoc testing was by Bonferroni adjustment (all tests were 2-tailed, α=0.05). Results: Before hemorrhage, the ETOH+ and ETOH– were evenly matched for lactate and MAP. Ethanol levels at tail amputation were 170±68 mg/dL. CHV (mL/100 g) were similar (P=.23) for the ETOH– (2.36±0.24) and ETOH+ (1.87±0.32) groups. No significant (P=1.00) difference was noted in posthemorrhage MAP between ETOH– (68.6±6.8 mmHg) and ETOH+ (69.3±7.2 mmHg) rats. The ETOH– group had a significantly (P<.032) higher lactate level (4.94 mmol/L±1.07 mmol/L) than the ETOH+ group (2.27 mmol/L±0.59 mmol/L). Conclusion: At this level of moderate ethanol intoxication, a lactic acidosis was not observed prehemorrhage. Posthemorrhage, ethanol intoxication may have ameliorated hemorrhagic shock, as evidenced by a lower level of arterial lactate.