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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1989-10-17
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pubmed:abstractText |
We studied whether enprostil, a synthetic prostaglandin E2 derivative, might inhibit gastrin release and the trophic effects on gastric oxyntic mucosa induced by prolonged treatment with an inhibitor of hydrogen-potassium-stimulated adenosine triphosphatase, the substituted benzimidazole BY 831-78. Rats were treated intragastrically with enprostil (1 or 15 micrograms/kg b.i.d.), BY 831-78 (15 mumol/kg once daily), the combination of enprostil and BY 831-78, ranitidine (300 mumol/kg b.i.d.), and placebo. Plasma gastrin and somatostatin levels and gastric acid secretion were measured during a 1-day treatment in animals fitted with chronic gastric fistulas and repeatedly during 9 wk of treatment in intact rats. Despite inhibiting acid secretion, enprostil did not increase plasma gastrin. When combined with BY 831-78, enprostil transiently reduced the BY 831-78-induced increase of integrated plasma gastrin (1375 +/- 206 vs. 2137 +/- 256 pmol/L.12 h, p less than 0.05) in fasted rats with fistulas, but failed to prevent the marked hypergastrinemia following 9 wk of treatment with BY 831-78 (717 +/- 80 vs. 731 +/- 56 pmol/L) in intact rats. However, enprostil reduced the BY 831-78-induced increase of oxyntic mucosal volume (458 +/- 31 vs. 567 +/- 33 mm3, p less than 0.01), whereas BY 831-78 prevented the enprostil-induced increase of antral mucosal volume (42 +/- 3 vs. 56 +/- 3 mm3, p less than 0.01). These results demonstrate that some of the trophic effects induced by a hydrogen-potassium-stimulated adenosine triphosphatase inhibitor are not exclusively governed by gastrin.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Enprostil,
http://linkedlifedata.com/resource/pubmed/chemical/Gastrins,
http://linkedlifedata.com/resource/pubmed/chemical/H( )-K( )-Exchanging ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E, Synthetic,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0016-5085
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
97
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
846-52
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2570729-Adenosine Triphosphatases,
pubmed-meshheading:2570729-Animals,
pubmed-meshheading:2570729-Benzimidazoles,
pubmed-meshheading:2570729-Enprostil,
pubmed-meshheading:2570729-Female,
pubmed-meshheading:2570729-Gastric Acid,
pubmed-meshheading:2570729-Gastric Mucosa,
pubmed-meshheading:2570729-Gastrins,
pubmed-meshheading:2570729-H(+)-K(+)-Exchanging ATPase,
pubmed-meshheading:2570729-Hydrogen-Ion Concentration,
pubmed-meshheading:2570729-Prostaglandins E, Synthetic,
pubmed-meshheading:2570729-Rats,
pubmed-meshheading:2570729-Rats, Inbred Strains,
pubmed-meshheading:2570729-Somatostatin
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pubmed:year |
1989
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pubmed:articleTitle |
Enprostil reduces the increase of gastric corpus mucosal mass induced by the hydrogen-potassium-stimulated adenosine triphosphatase inhibitor BY 831-78 in the rat.
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pubmed:affiliation |
Gastrointestinal Unit, University Hospital, Inselspital, Bern, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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