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 PGE2α 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.
|Original language||English (US)|
|Number of pages||5|
|Journal||Prostaglandins, Leukotrienes and Essential Fatty Acids|
|State||Published - Apr 1990|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology