Prostaglandin synthesis inhibition and postprandial intestinal hyperemia.
The effect of prostaglandin synthesis inhibition on the postprandial intestinal hyperemia was examined in the jejunum of anesthetized dogs. Both intravenous and intra-arterial infusion of the cyclooxygenase inhibitors indomethacin and mefenamic acid reduced resting jejunal blood flow and markedly enhanced the food-induced jejunal hyperemia. The jejunal vascular response to food did not change after either intravenous or intra-arterial infusion of the carrier solutions or intra-arterial infusion of angiotensin II. The enhancement of the jejunal hyperemia was associated with an increase in the food-induced increase in jejunal oxygen consumption. Infusion of the cyclooxygenase inhibitors increased the mean amplitude of the monophasic intestinal contractions; however, this did not appear to play a role in the enhancement of the food-induced hyperemia. The study indicates that inhibition of prostaglandin synthesis has a marked effect on the postprandial intestinal hyperemia and that this may be due to its enhancement of the jejunal metabolic response to food. The prostaglandins involved and their mechanism of action are unknown.
D000818:Animals; D004285:Dogs; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D006940:Hyperemia / Q000503:physiopathology; D007213:Indomethacin / Q000494:pharmacology*; D007583:Jejunum / Q000098:blood supply*; D008297:Male; D008528:Mefenamic Acid / Q000494:pharmacology*; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011453:Prostaglandins / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects
D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D008528:Mefenamic Acid; D007213:Indomethacin