Prostanoid Synthesis by Cultured Gastric and Duodenal Mucosa: Possible Role in the Pathogenesis of Duodenal Ulcer

P. Sharon Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

F. Cohen Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

A. Zifroni Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

F. Karmeli Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

M. Ligumsky Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

D. Rachmilewitz Dept. of Gastroenterology, Hadassah University Hospital, The Hebrew University Hadassah Medical School, Jerusalem, and the Dept. of Hormone Research, Weizmann Institute of Science, Rehovoth, Israel

Abstract

Cultured duodenal mucosa obtained from normal subjects synthesized and secreted significantly less prostaglandin E₂ (PGE₂), 6-keto-PGF_1α, and thromboxane B₂ (TXB₂) than cultured gastric mucosa obtained from the same subjects. Accumulation of PGE₂, 6-keto-PGF_1α, and TXB₂–the stable metabolites of prostacyclin I₂ and thromboxane A₂, respectively–by cultured gastric mucosa obtained from 21 untreated patients with active duodenal ulcer was significantly lower than their respective accumulation by cultured gastric mucosa obtained from 14 normal subjects. Accumulation of all three prostanoids by cultured duodenal mucosa obtained from patients with active duodenal ulcer and from normal subjects was not significantly different. PGE₂, 6-keto-PGF_1α, and TXB₂ accumulation was five to six times higher than their respective content in fresh tissue before culture and was inhibited by flufenamic acid. These results suggest that a decrease in endogenous gastric prostanoid synthesis may have a role in the pathogenesis of peptic ulcer disease.

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Prostanoid Synthesis by Cultured Gastric and Duodenal Mucosa: Possible Role in the Pathogenesis of Duodenal Ulcer

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Prostanoid Synthesis by Cultured Gastric and Duodenal Mucosa: Possible Role in the Pathogenesis of Duodenal Ulcer

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