Hemodynamic and metabolic effects of ethanol in canine hemorrhagic shock

Abstract

Ethanol has been reported to cause myocardial suppression, exaggerated hypotension, and increased mortality in various animal models of hemorrhagic shock. Previous studies have not used a fixed-volume graded hemorrhage model and have not monitored cardiac output or metabolic parameters such as serum glucose and lactate levels. We studied hemodynamic and metabolic changes after administration of ethanol in a 50% graded hemorrhage model in conditioned, anesthetized beagles after orogastric ethanol loading. The hemorrhage was done over a 60-min period followed by a 90-min stabilization period. The ethanol group (n = 6) had significantly higher heart rates during the stabilization period. Mean arterial pressures (MAP) were lower in the ethanol group during the stabilization period. The change from baseline MAP 30 min after hemorrhage was -31% in the control group and -53% in the ethanol group (P less than .05 using Wilcoxon ranked sum test). Serum glucose and lactate levels were higher in the ethanol group. These results indicate that ethanol impairs hemodynamics and alters glucose and lactate metabolism in dogs in the fixed-volume graded hemorrhage model. The effect of these changes on morbidity and mortality remains to be determined.