Abstract
The mechanism of endotoxemia-induced alterations in gastrointestinal motility still remains unclear. The aim of the present study was to investigate the effect of bacterial lipopolysaccharide (LPS) on contractility of gastric fundus. Endotoxemia was induced by single injection of LPS (10 mg/kg) in mice. In vitro exposure to LPS was performed using rat gastric fundus. In vivo gastric emptying was measured in mice using the phenol red method. LPS induced significant reduction of electrically induced contractions of mouse gastric fundus. The effect of LPS was diminished by tumor necrosis factor alpha (TNF-α) production inhibitor, recombinant human lactoferrin. LPS inhibited responses to prostaglandin F 2 α (PGF 2 α ) and 5-hydroxytryptamine (5-HT) but not to acetylcholine (ACh). Similar effects were observed after incubation of tissue with LPS. 5-HT- and KCl-induced contractions were smaller in tissues incubated with LPS for 8 h while response to ACh was not significantly changed. Gastric emptying was inhibited during endotoxemia. However at the time when maximal decrease in gastric fundus contractility was observed (8 h) gastric emptying was with control value. In conclusion, the effect of LPS on gastric motoric function is due to central and local actions of endotoxin and is mediated by TNF-α production.
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