2012 Volume 37 Issue 3 Pages 649-654
Endotoxin-induced shock, which is a common problem in the intensive care unit, has a high mortality rate. Cytokines produced from leukocytes that are activated by endotoxins have been implicated in the pathophysiology of endotoxin-induced shock. The present study was conducted in order to clarify the effects of acute low-dose ethanol administration on endotoxin-induced shock and cytokine responses in rats. Twenty rats were randomly assigned to 4 groups: control group received saline, ethanol group received acute low-dose ethanol (100 mg•kg-1•hr-1 for 2 hr, i.v.), endotoxin group received endotoxin (Escherichia coli lipopolysaccharide; 15 mg/kg, i.v.), and endotoxemia-ethanol group received acute low-dose ethanol after the injection of endotoxin. After the endotoxin injection, hemodynamics, acid-base statuses, and the plasma concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 were assessed in each of the 4 groups. The systolic arterial pressure was significantly greater in endotoxemia-ethanol group than in endotoxemia group from 0.5 to 1.0 hr after injection. The base excess was significantly greater in endotoxemia-ethanol group than in endotoxemia group from 3 to 4.5 hr after injection. Plasma TNF-α concentration in endotoxemia-ethanol group was significantly lower than that in endotoxemia group 3 hr after injection, and plasma IL-10 concentration in endotoxemia-ethanol group was significantly higher than that in endotoxemia group from 3 to 4.5 hr after injection. Acute low-dose ethanol administration inhibited endotoxin-induced shock, metabolic acidosis, inflammatory cytokine responses, and activated anti-inflammatory cytokine responses in rats.