Background: Recent advances in endoscopy have revealed that NSAIDs often cause ulcers in the human small intestine. However, the mechanism of intestinal ulcer formation is still unclear.
Aims: The role of dietary fiber (DF), intestinal motility and leukotrienes (LTs) in the formation of small intestinal ulcers induced by indomethacin (IND) was investigated in cats.
Methods: Several types of diets containing DF at various percentages were given to animals twice daily during the experiment. IND was administered orally once daily after the morning meal for 3 days, and the area of mucosal lesions in the intestine was measured. Gastrointestinal motility was measured using a telemetry system in conscious cats implanted with force transducers.
Results: In cats fed regular dry food containing 2.8% DF, IND (3 mg/kg, p.o.) significantly increased the motility of the lower half of the small intestine and produced many severe lesions; the total lesion area was 7.7±2.0 cm2 (n=5). The lesions were markedly decreased with the low (0.4%)-DF diet and increased with the high (7.2%)-DF diet. The lesion area was 0.1±0.1 cm2 (P<0.05) and 18.2±4.1 cm2 (P<0.05), respectively. Supplementation with insoluble DF (6% cellulose), but not soluble DF (pectin), in the low-DF diet increased the lesion area significantly. The hypermotility and lesion formation in the small intestine induced by IND were significantly (P<0.05) inhibited by AA-861 (a 5-lipoxygenase inhibitor), pranlukast (a LT receptor antagonist), or atropine.
Conclusions: Insoluble DF, intestinal hypermotility, leukotrienes and cholinergic pathways are implicated in the pathogenesis of small intestinal ulcers induced by NSAIDs.
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