Open AccessTumour necrosis factor mediates bacterial translocation after haemorrhagic shock and endotoxaemia
Author(s) -
Goldman Gideon,
Soffer Dror,
Heller Leor,
Aderka Dan,
Lahat Adi,
Klausner Joseph M.
Publication year - 2001
Publication title -
european journal of surgery
Language(s) - English
Resource type - Journals
eISSN - 1741-9271
pISSN - 1102-4151
DOI - 10.1080/110241501300091543
Subject(s) - chromosomal translocation , tumor necrosis factor alpha , medicine , shock (circulatory) , lipopolysaccharide , bacterial translocation , necrosis , endotoxic shock , immunology , endocrinology , biology , biochemistry , gene
Objective: To assess the extent of bacterial translocation after haemorrhagic shock and reperfusion, and the involvement of tumour necrosis factor (TNF) in its mediation. Design: Controlled, randomised prospective experiment. Subjects: 87 rats in 7 groups Interventions: Haemorrhagic shock was induced in rats for 1 hour. Endotoxaemia was induced in a second group by the injection of lipopolysaccharide. A third group was injected with exogenous TNF. Some of the animals were further treated with anti‐TNF. Measurements: After 24 hours, bacterial translocation in blood and in several remote organs, and serum TNF concentrations were measured. Results: High bacterial counts were found in all remote organs of rats with haemorrhagic shock or endotoxaemia. Their serum TNF concentrations were significantly higher than in the corresponding sham‐operated controls. Anti‐TNF significantly reduced the extent of bacterial translocation. Rats, the only treatment of which was exogenous TNF, developed substantial bacterial translocation. Conclusion: Bacterial translocation is associated with increased serum TNF, and can be minimised by anti‐TNF. This, and the triggering of translocation in unprovoked animals by TNF alone, suggest that TNF may be the stimulator, and not the consequence, of bacterial translocation. Copyright © 2001 Taylor and Francis Ltd.