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

Abstract

Cultured duodenal mucosa obtained from normal subjects synthesized and secreted significantly less prostaglandin E2 (PGE2), 6-keto-PGF1.alpha. and thromboxane B2 (TXB2) than cultured gastric mucosa obtained from the same subjects. Accumulation of PGE2, 6-keto-PGF1.alpha. and TXB2, the stable metabolites of prostacyclin I2 and thromboxane A2, respectively.sbd.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 3 prostanoids by cultured duodenal mucosa obtained from patients with active duodenal ulcer and from normal subjects was not significantly different. PGE2, 6-keto-PGF1.alpha. and TXB2 accumulation was 5-6 times higher than their respective content in fresh tissue before culture and was inhibited by flufenamic acid. A decrease in endogenous gastric prostanoid synthesis may have a role in the pathogenesis of peptic ulcer disease.