Protective effects of prostaglandins in the isolated gastric mucosa of eel, Anguilla anguilla

The protective effect of endogenous prostaglandins on the fish gastric mucosa was evaluated by studying the effect of indomethacin and aspirin, known cyclooxigenase inhibitors, on the mucosal ulceration in the isolated gastric sacs of Anguilla anguilla. Gastric sacs devoid of muscle layers were incu...

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Bibliographic Details
Main Authors: TRISCHITTA, Francesca Ross, DENARO, Maria Gabr., FAGGIO, Caterina, MANDOLFINO, Mattia Grazia
Other Authors: Trischitta, Francesca Ro, Denaro, Maria Gabr., Faggio, Caterina, Mandolfino, Mattia Grazia
Format: Article in Journal/Newspaper
Language:unknown
Published: 1998
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Online Access:http://hdl.handle.net/11570/1889338
http://ISI PT: J, DT: Meeting Abstract
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Summary:The protective effect of endogenous prostaglandins on the fish gastric mucosa was evaluated by studying the effect of indomethacin and aspirin, known cyclooxigenase inhibitors, on the mucosal ulceration in the isolated gastric sacs of Anguilla anguilla. Gastric sacs devoid of muscle layers were incubated in the presence of indomethacin (10-4 mol · 1-1) or aspirin (10-4 mol · 1-1) in different experimental conditions. Both the anti-inflammatory drugs produced ulcers, but the effects were more severe in the presence of histamine and in the absence of HCO3/- in the incubation bath. The effects of prostaglandin E2 (PGE2) on acid secretion rate (J(H)) and on alkaline secretion rate (J(OH)) were evaluated (with the aid of the pH stat method) in isolated gastric mucosa mounted in Ussing chambers. We found that PGE2 (10-8-10-5 mol · 1-1) increased J(H) in a dose-dependent manner. In tissues pretreated with luminal omeprazole (10-4 mol · 1-1), PGE2 stimulated gastric alkaline secretion. It was nullified by serosal removal of HCO3/- or Na+ and by serosal ouabain (10-4 mol · 1-1). These results suggested that prostaglandins also exert their protective effects in fish gastric mucosa. This protection seems partially due to a stimulation of exogenous HCO3/- transport from the serosal to the mucosal side. It is likely that this transport is an active transcellular mechanism coupled to Na+ transport.