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Endotoxin Actions on Myoelectric Activity, Transit, and Neuropeptides in the Gut (Role of Nitric Oxide)

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Abstract

The lipopolysaccharide (endotoxin) ofgram-negative bacteria has systemic effects in animalsand man. Our aim was to investigate the effects of E.coli lipopolysaccharide on motility and transit through the small intestine in rats and to analyzeplasma and tissue concentrations of intestinalneuropeptides. When lipopolysaccharide (20–160μg/kg) was administered intravenously, the migratingmyoelectric complex was replaced by spike burstsaccompanied by rapid transit. Tissue concentrations ofsubstance P and neurokinin A decreased, while plasmalevels of calcitonin gene-related peptide increased.Nω-Nitro-L-arginine, Nω-L-arginine methyl ester,dexamethasone, or indomethacin prevented these changesin myoelectric activity and tissue contents ofneuropeptides. All of these compounds, exceptindomethacin, prevented the increased rate of transit. Thus,lipopolysaccharide changes motility through the nitricoxide and arachidonic pathways, resulting in rapidtransit through the gut.

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Hellstrom, P.M., Al-Saffar, A., Ljung, T. et al. Endotoxin Actions on Myoelectric Activity, Transit, and Neuropeptides in the Gut (Role of Nitric Oxide). Dig Dis Sci 42, 1640–1651 (1997). https://doi.org/10.1023/A:1018897028463

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