This study examined whether acute alcohol (EtOH) intoxication before
burn injury potentiates postburn intestinal tissue damage and whether neutrophils have any role in the damage under those conditions. Male rats ( approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL or with saline and received either approximately 12.5% or approximately 25% total body surface area (TBSA)
burn or
sham injury. Rats were killed at 4 or 24 h after injury, and various parameters were measured. As compared with
sham animals,
burn injury alone (regardless of size) resulted in a significant increase in intestinal tissue
myeloperoxidase (MPO; an index of neutrophil infiltration) activity and
IL-18 levels 4 h after injury. Furthermore, rats receiving 25% TBSA, but not 12.5%,
burn exhibited intestine
edema. The
IL-18 and MPO activity were normalized at 24 h after injury in rats receiving 12.5% TBSA
burn, whereas these parameters remained elevated at 24 h in rats with 25%
burn. The presence of EtOH in rats at the time of
burn injury exacerbated the levels of
IL-18, MPO activity, and
edema at 4 and 24 h after
burn injury. Treatment of rats with anti-IL-18
antibodies or with antineutrophil antiserum prevented the increase in the above parameters after EtOH and
burn injury, except that the depletion of neutrophils did not prevent the
IL-18 increase. In summary, these findings suggest that acute EtOH intoxication exacerbates postburn intestinal tissue damage after
burn injury, and that it is, in part, neutrophil mediated.