Papel de la ciclooxigenasa (COX) en las alteraciones motoras gastrointestinales y la fiebre inducidas por el lipopolisacárido (LPS) en la oveja / No disponible

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Role of prostaglandins in lipopolysaccharide effects on K+-induced contractions in rabbit small intestine.

AIM: The mediators of the pathophysiologcal symptoms of septic shock are not completely understood. The aim of this work was to investigate the effect of lipopolysaccharide (LPS) on the K+-induced response of longitudinal segments of rabbit small intestine in vitro and the possible role of prostaglandins. METHODS AND RESULTS: Rabbits were treated with intravenously injected LPS. After 90 min animals were killed and intestinal segments were mounted in an organ bath. Lipopolysaccharide (0.2 microg kg-1) inhibited K+-induced contractions (60 mm) by 68% in duodenum, 58% in jejunum and 52% in ileum. Indomethacin antagonized LPS actions when injected 15 min before LPS. PGE2 reduced K+-induced contractions, imitating LPS effects. In contrast, contractions induced by K+ increased when intestinal segments were incubated in vitro with LPS for 90 min. The LPS (0.3 microg mL-1) increased K+-induced contractions (60 mm) by 46% in duodenum, 63% in jejunum and 85% in ileum. The LPS effect was antagonized by indomethacin at 10-6 m in duodenum and jejunum and at 10-8 m in ileum. PGE2 evoked dose-dependent contractions when added to the bath in duodenum, jejunum and ileum. CONCLUSION: These results suggest that effect of LPS on K+-induced contractions in the rabbit small bowel may be mediated by prostaglandin E2.

Central tumour necrosis factor-alpha mediates the early gastrointestinal motor disturbances induced by lipopolysaccharide in sheep.

Cytokines are involved in fever and other symptoms of the acute phase response induced by endotoxins. The aim of this work was to study the involvement of central tumour necrosis factor-alpha (TNF-alpha) in the changes induced by lipopolysaccharide (LPS) on gastrointestinal (GI) motility in sheep. Body temperature and myoelectric activity of the antrum, duodenum and jejunum was recorded continuously. Intravenous (i.v.) administration of LPS (0.1 micro g kg-1)-induced hyperthermia, decreased gastrointestinal myoelectric activity and increased the frequency of the migrating motor complex (MMC). These effects started 40-50 min after LPS and lasted for 6-7 h. TNF-alpha (50 and 100 ng kg-1) mimicked these effects when injected intracerebroventricularly (i.c.v.) but not i.v. Pretreatment with soluble recombinant TNF receptor (TNFR:Fc, 10 micro g kg-1, i.c.v.) abolished the TNF-induced actions and reduced those evoked by LPS. Furthermore, the effects induced by either LPS or TNF were suppressed by prior i.c.v. injection of indomethacin (100 micro g kg-1). In contrast, the i.v. injections of TNFR:Fc or indomethacin were ineffective. Our data suggest that LPS disturbs GI motility in sheep through a central pathway that involves TNF-alpha and prostaglandins sequentially.

Effect of motilin on gastrointestinal myoelectric activity in conscious rabbits.

Gastrointestinal myoelectric activity was investigated in conscious rabbits with chronically implanted electrodes. As rabbit stomach is never empty, food was removed 1 h before the beginning of recordings. Propagated activity fronts spontaneously started in the jejunum without associated changes in the antroduodenal area. Intravenous administration of either motilin (600-1500 ng/kg) or erythromycin (5-50 micrograms/kg) did not modify antral activity, but simultaneously increased duodenal and jejunal activity in a dose-dependent manner. Spontaneous and induced jejunal activity fronts showed some similarities. However, those induced did not propagate and were not followed by a quiescence period. The effects of motilin (900 ng/kg) and erythromycin (25 micrograms/kg) were resistant to atropine (0.5 mg/kg), hexamethonium (2 mg/kg), or ondansetron (0.5 mg/kg). These results suggest that motilin is not a physiological modulator of the migrating myoelectric complex (MMC) in rabbits. Moreover, neither cholinergic nor 5-HT3 receptors are involved in either motilin or erythromycin-induced actions.