Role of arachidonic acid metabolites in acid-pepsin injury to rabbit esophagus
1989; Elsevier BV; Volume: 97; Issue: 2 Linguagem: Inglês
10.1016/0016-5085(89)90062-0
ISSN1528-0012
AutoresBruce E. Stein, Michal L. Schwartzman, Mairéad A. Carroll, Rosalyn E. Stahl, William S. Rosenthal,
Tópico(s)Gastroesophageal reflux and treatments
ResumoThe role of cyclooxygenase and lipoxygenase metabolites of arachidonic acid in experimental esophageal were lumenally perfused for 1 h with acidified saline (pH 2.0) with or without pepsin followed by a second hour with acidified saline. Separate groups of pepsin-perfused animals were pretreated with indomethacin, a cyclooxygenase inhibitor, or BW755C, a lipoxygenase-cyclooxygenase inhibitor. Esophageal injury was graded grossly. H+ and hemoglobin fluxes were determined. Acidified saline caused no significant damage. Pepsin induced moderate injury. Indomethacin decreased pepsin-induced H+ flux by 55% without affecting the other indices. BW755C, by all measurements, dramatically increased pepsin-induced injury. In separate experiments, cyclooxygenase activity was decreased by indomethacin and BW755C by 62% and 49%, respectively. Lipoxygenase activity was decreased 74% by BW755C and was not significantly affected by indomethacin. These results suggest that esophageal cytoprotection is mediated by endogenous lipoxygenase metabolites.
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