Effect of ethanol on lactic acidosis in experimental hemorrhagic shock.
Many trauma victims who have hemorrhagic shock are also intoxicated. Ethanol could worsen the severity of shock and decrease the amount of blood loss necessary to reach or maintain the shock state, perhaps by increasing lactic acidosis. We examined the effect of ethanol on lactic acidosis in a group of rats that were intoxicated, then put in a state of hemorrhagic shock (MAP = 40 mm Hg). These animals were compared to a control group that were in a similar state of hemorrhagic shock but not intoxicated. The volumes of blood necessary to reach and maintain the predetermined model state of shock for two hours in each group were also measured. The animals were paralyzed and placed on controlled ventilation. The ethanol produced an expected baseline lactic acidosis, and it took significantly less blood volume loss to keep the intoxicated group in shock. However, during shock there was no significant difference in the state of lactic acidosis. These results suggest that acute ethanol intoxication made the animals more sensitive to hemorrhage. This effect was not mediated by an increase in lactic acidosis in our model.
D000138:Acidosis / Q000097:blood / Q000209:etiology*; D000435:Alcoholic Intoxication / Q000097:blood / Q000150:complications*; D000818:Animals; D001784:Blood Gas Analysis; D000431:Ethanol / Q000097:blood; D006801:Humans; D007773:Lactates / Q000097:blood*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000097:blood / Q000150:complications*
D007773:Lactates; D000431:Ethanol