• Xiaoling Li, Martin G Schwacha, Irshad H Chaudry, and Mashkoor A Choudhry.
• Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
• Shock. 2008 Mar 1;29(3):377-83.

AbstractThis 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.

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