Acute alcohol intoxication potentiates neutrophil-mediated intestinal tissue damage after burn injury

Academic Article


  • 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 (∼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. ©2008The Shock Society.
  • Authors

    Published In

  • Shock  Journal
  • Digital Object Identifier (doi)

    Author List

  • Li X; Schwacha MG; Chaudry IH; Choudhry MA
  • Start Page

  • 377
  • End Page

  • 383
  • Volume

  • 29
  • Issue

  • 3