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The role of cyclooxygenase inhibitors in repair of ischaemic‐injured jejunal mucosa in the horse
Author(s) -
CAMPBELL N. B.,
BLIKSLAGER A. T.
Publication year - 2000
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.2000.tb05335.x
Subject(s) - etodolac , cyclooxygenase , prostaglandin , pharmacology , horse , jejunum , prostaglandin e2 , medicine , chemistry , biology , biochemistry , enzyme , paleontology
Summary Cyclooxygenase inhibitors are administered to horses to prevent endotoxin‐induced elaboration of prostaglandins. However, PGE 2 and PGI 2 stimulate repair of injured intestine. There are 2 isoforms of cyclooxygenase: COX‐1, which constitutively produces prostaglandins and COX‐2, which is induced by inflammation. We hypothesised that the nonspecific cyclooxygenase inhibitor flunixin meglumine would retard repair of ischaemic intestinal injury by preventing production of reparative prostaglandins, whereas the selective COX‐2 inhibitor, etodolac, would permit repair as a result of continued COX‐1 prostaglandin production. Segments of equine jejunum were subjected to ischaemia for 1 h, and recovered for 4 h in Ussing chambers. In ischaemic tissue, treated with the nonspecific cyclooxygenase inhibitor, flunixin meglumine (2.7 times 10 −5 mol/1), production of PGE 2 and PGI 2 was inhibited, and there was no evidence of recovery based on measurements of transepithelial resistance. Conversely, untreated ischaemic tissues or tissues treated with the specific COX‐2 inhibitor etodolac (2.7 times 10 −5 mol/1) had significant elevations in PGE 2 and PGI 2 , and significant recovery of transepithelial resistance. These studies suggest that specific COX‐2 inhibitors may provide an advantageous alternative to nonspecific cyclooxygenase inhibitors in horses with colic.