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A Rat Model of Ischemic Enteritis: Pathogenic Importance of Enterobacteria, iNOS/NO, and COX‐2/PGE2

We investigated the roles of prostaglandins (PGs), nitric oxide (NO) and enterobacteria in a model of ischemic enteritis. Under ether anesthesia, ischemic enteritis was induced in 18 h‐fasted rats by a stenosis in the superior mesenteric artery (SMA) that was produced by placing a needle (23 guage) on the vessel, ligating both the vessel and needle, and then removing a needle from the ligature. After operation, the animals were fed normally and killed 3 days after surgery. Various drugs were given once daily for 2 days after the operation. Stenosis of the SMA produced hemorrhagic enteritis on the anti‐mesenteric side of the small intestine. The occurrence of enteritis was accompanied by enterobacterial invasion and the upregulated expression of iNOS/NO as well as COX‐2/PGE2 in the mucosa. The enteritis was prevented by ampicillin, L‐NAME or aminoguanidine, while aggravated by indomethacin, rofecoxib or an EP4 antagonist. The deleterious effect of indomethacin was antagonized by the co‐administration of PGE2 or an EP4 agonist. These results suggest that enterobacteria played a major pathogenic role in this model of ischemic enteritis, and also that iNOS/NO was deleterious in the pathogenesis of these lesions, while COX‐2/PGE2 prevented the development of ischemic enteritis by activating EP4 receptors.