Prostaglandin E₂ formation by rat gastroduodenal tissue following intragastric acid perfusion

Rat gastroduodenal mucosa forms prostaglandin (PG) E₂. However, little is known about regional differences in PGE₂ formation or the effect of gastric hydrochloric acid (HCl) perfusion on regional PGE₂ formation. In this study, the rats were divided into 3 groups. Group 1 received intravenous (i.v.), 1 ml/h, and intragastric (i.g.), 8 ml/h, perfusions of saline simultaneously for 3 h. Group 2 received saline i.v. and 0.15 N HCl i.g., 8 ml/h. Group 3 was injected with a bolus of aspirin (ASA), 60 mg/kg, followed by ASA, 40 mg/kg/h i.v., and 0.15 N HCl i.g.. The gastric aspirates were analyzed for volume and pH. Segments of gastroduodenal tissue from the fundus, corpus, antrum, and duodenum were minced and then incubated in 1 ml of 50 mM Tris buffer, pH 8.4, for 30 sec with mixing; the incubate was assayed for PGE₂ by radioimmunoassay. Intragastric HCl decreased the pH of aspirate without producing gastric mucosal lesions. However, when combined with i.v. ASA, ulcer formation was present in all animals (p < 0.05). PGE₂ was formed by isolated tissue from four different gastroduodenal regions. The duodenum formed significantly greater amounts than the fundus, antrum, or corpus, which were similar. Intragastric HC1 produced a trend toward increased PGE₂ formation (pmol PGE₂/mg tissue) in the fundus, 143 ± 36 to 237 ± 57; corpus, 87 ± 13 to 200 ± 57; antrum, 157 ± 28 to 224 ± 65; and duodenum, 235 ± 56 to 338 ± 51. However, statistical significance was not reached. Intragastric HC1 combined with i.v. ASA reduced PGE₂ formation by tissue from all four regions below detectable levels. The data indicate that PGE_2α formation by rat gastroduodenal tissue differs regionally, and i.g. HCl perfusion did not significantly increase PGE₂ formation. However, when i.g. HCl perfusion combined with i.v. ASA, the PGE₂ formation was reduced below detectable levels.