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

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
Published in:Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology
Main Authors: FAGGIO, Caterina, DENARO, Maria Gabr., TRISCHITTA, Francesca Ross, LIONETTO, M. G.
Other Authors: FAGGIO, C., DENARO, M. G., TRISCHITTA, F.
Format: Article in Journal/Newspaper
Language:unknown
Published: 2000
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Online Access:http://hdl.handle.net/11570/1602996
https://doi.org/10.1007/s003600000111
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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.l(-1)) or aspirin (10(-4) mol.l(-1)) in different experimental conditions. Both the antiinflammatory 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 E-2 (PGE(2)) on acid secretion rate (JH) 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 PGE(2) (10(-8)-10(-5) mol.l(-1)) increased JH in a dose-dependent manner. In tissues pretreated with luminal omeprazole (10(-4) mol.l(-1)), PGE2 stimulated gastric alkaline secretion. It was nullified by serosal removal of HCO; or Nat and by serosal ouabain (10(-4) mol.l(-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.