Effect of exogenous and endogenous prostaglandin e upon gastric endocrine function in dogs

The effects of prostaglandin E₂ (PGE₂) and indomethacin- induced endogenous PGE deficiency upon basal and postprandial release of gastric somatostatin-like immunoreactivity (SLI), glucagon, and gastrin during the gastric phase of a meal were determined in anesthetized, laparotomized dogs. The infusion of PGE₂ (1 μg/kg- min) elicited a sustained rise in antral vein and inferior vena cava plasma SLI levels and a transient SLI rise in the fundic vein. Antral vein and inferior vena cava gastrin decreased significantly during PGE₂ infusion, while fundic vein and inferior vena cava glucagon rose significantly. Indomethacin infusion (2 mg/kg-h) elicited a significant decrease in basal SLI levels in the fundic and antral veins and in the inferior vena cava plasma and a significant increase in basal antral vein gastrin levels, but no change in basal inferior vena cava gastrin or in basal fundic vein or inferior vena cava glucagon levels. The effects of PGE₂ infusion upon postprandial SLI, gastrin, and glucagon varied with the intragastric pH. When infused during a liver meal at pH 7, PGE₂ (1 μg/kg-min) abolished both the modest rise in fundic, antral, and inferior vena cava plasma SLI levels and the increase in antral and inferior vena cava gastrin levels and reduced the fundic glucagon release. When infused during a liver meal at pH 2, PGE₂ reduced the large rise in antral vein SLI and abolished the decrease in fundic vein SLI but did not alter either the small increase in gastrin or the release of gastric glucagon. Indomethacin infusion during the liver meal at pH 7 did not affect the antral vein SLI response, but the fundic vein SLI response was abolished and the rise in inferior vena cava SLI was reduced; antral vein and inferior vena cava gastrin levels were significantly higher, while glucagon did not change. Indomethacin infusion during a meal at pH 2 reduced antral vein and inferior vena cava SLI for the first 20 min, while fundic vein SLI levels rose significantly, in contrast to a decrease observed in the controls. Antral and inferior vena cava gastrin levels rose significantly, in contrast to the control response, and the inhibition of gastrin release induced by intragastric acidification was abolished during indomethacin infusion, as was the acid-induced reduction in gastric glucagon release. It is concluded that exogenously administered PGE₂ affects the basal and postprandial release of SLI, gastrin, and glucagon from the stomach. Endogenous PGs may be important in the regulation of basal and postprandial gastric endocrine function.