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A Rat Model of Ischemic Enteritis: Pathogenic Importance of Enterobacteria, iNOS/NO, and COX‐2/PGE 2
Author(s) -
Takeuchi Koji,
Komatsu Yoshino,
Kotani Tohru
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1067.7
Subject(s) - enteritis , medicine , nitric oxide , pathogenesis , agonist , radiation enteritis , gastroenterology , pharmacology , endocrinology , receptor
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/PGE 2 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 PGE 2 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/PGE 2 prevented the development of ischemic enteritis by activating EP4 receptors. Support or Funding Information none