作者: N. B. CAMPBELL , A. T. BLIKSLAGER
DOI: 10.1111/J.2042-3306.2000.TB05335.X
关键词:
摘要: Summary Cyclooxygenase inhibitors are administered to horses prevent endotoxin-induced elaboration of prostaglandins. However, PGE2 and PGI2 stimulate repair injured intestine. There 2 isoforms cyclooxygenase: COX-1, which constitutively produces prostaglandins COX-2, is induced by inflammation. We hypothesised that the nonspecific cyclooxygenase inhibitor flunixin meglumine would retard ischaemic intestinal injury preventing production reparative prostaglandins, whereas selective COX-2 inhibitor, etodolac, permit as a result continued COX-1 prostaglandin production. Segments equine jejunum were subjected ischaemia for 1 h, recovered 4 h in Ussing chambers. In tissue, treated with (2.7 times 10−5 mol/1), was inhibited, there no evidence recovery based on measurements transepithelial resistance. Conversely, untreated tissues or specific etodolac mol/1) had significant elevations PGI2, These studies suggest may provide an advantageous alternative colic.