Differential effects of prostaglandins and arachidonic acid on gastric circulation and oxygen consumption

• Published in: Prostaglandins Vol. 20; no. 6; p. 1089
• Main Authors: Walus, K M, Gustaw, P, Konturek, S J
• Format: Journal Article
• Language: English
• Published: United States 01-12-1980
• Subjects: Animals; Arachidonic Acids - pharmacology; Dogs; Epoprostenol - pharmacology; Female; Histamine - pharmacology; Indomethacin - pharmacology; Male; Oxygen Consumption - drug effects; Perfusion; Prostaglandins - pharmacology; Prostaglandins E - pharmacology; Regional Blood Flow; Stomach - blood supply
• ISSN: 0090-6980
• DOI: 10.1016/0090-6980(80)90062-3

Experiments were carried out on anesthetized dogs to compare the effects of prostaglandin E2 (PGE2), prostacyclin (PGI2) and arachidonic acid (AA) administered intraarterially on gastric blood flow and oxygen consumption during constant arterial pressure perfusion and constant flow perfusion of the stomach. Both PGE2 and PGI2 increased total blood flow and oxygen consumption both in the resting stomach and following histamine stimulation although the effects of PGE2 on the oxygen consumption in stimulated stomach were not statistically significant. On the contrary, AA decreased both gastric blood flow and oxygen consumption in the histamine stimulated stomach. To determine if these compounds can influence gastric oxygen consumption independently of their effects on blood flow, the experiments with constant flow perfusion were performed. Both PGE2 and PGI2 decreased both the perfusion pressure and oxygen consumption in the resting as well as in the histamine-stimulated stomach whereas AA increased perfusion pressure and decreased oxygen consumption during histamine administration. Effects of AA were blocked by indomethacin suggesting that not AA itself but some of its metabolites, most likely thromboxanes were responsible for the hemodynamic and metabolic changes resulting from the contraction of gastric arterioles and precapillary sphincters. On the contrary, both PGE2 and PGI2 caused gastric hyperemia and an increase in oxygen consumption in the resting stomach, but decreased the latter parameter in the stimulated stomach, most probably as a result of secretory inhibition overcoming direct vascular effects of these compounds.