Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation

Surgery. 1988 Aug;104(2):191-8.

Abstract

Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after hemorrhage and reinfusion, the mesenteric lymph node, liver, and spleen were harvested from each animal for bacterial culture, and the ileum and cecum were examined histologically. Sham-shocked (control) rats were instrumented, but blood was not withdrawn. The incidence of BT was higher in the shocked rats (61%) than in the sham-shocked animals (7%) (p less than 0.01). Allopurinol (50 mg/kg, administered orally), a competitive inhibitor of xanthine oxidase, reduced the incidence of shock-induced BT to 14% (p = 0.02). Similarly, rats fed a tungsten-supplemented molybdenum-free diet, which inactivates xanthine oxidase, reduced shock-induced BT to 10% (p = 0.02). The histologic damage cause by hemorrhagic shock was prevented by blocking xanthine oxidase activity. Thus hemorrhagic shock-induced bacterial translocation from the gut appears to be mediated by oxidants generated by activation of the xanthine oxidase system.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Allopurinol / pharmacology
  • Animals
  • Diet
  • Enzyme Activation / drug effects
  • Intestines / microbiology*
  • Intestines / pathology
  • Liver / microbiology
  • Lymph Nodes / microbiology
  • Male
  • Peritoneal Cavity / microbiology
  • Rats
  • Rats, Inbred Strains
  • Shock, Hemorrhagic / physiopathology*
  • Spleen / microbiology
  • Tungsten / pharmacology
  • Xanthine Oxidase / antagonists & inhibitors*

Substances

  • Allopurinol
  • Xanthine Oxidase
  • Tungsten