The role of prostacyclin (PGI2) in metabolic hyperemia.
We explored the possibility that prostacyclin might be the dilator metabolite of postprandial hyperemia. In canine free-flow preparations, effects of prostacyclin were compared with effects of actively absorbed nutrients on hemodynamic and metabolic parameters in the small intestine. Prostacyclin was infused directly into the superior mesenteric artery for 10 minutes at 1.0 nanograms/kg-min. In absorptive study an isosmotic solution of glucose (1.0 g/l) dissolved in 0.9% NaCl was perfused through the gut lumen for 20 minutes. Prostacyclin increased total blood flow to the intestinal segment and decreased oxygen extraction, while not significantly changing either oxygen consumption or PS-product. Active cotransport of glucose and sodium increased total blood flow, oxygen extraction, oxygen consumption and PS-product. In constant flow canine gut preparations, intraarterial prostacyclin infusion decreased arterial pressure, oxygen extraction, oxygen consumption and mesenteric vascular resistance but increased venous pressure. Absorption of glucose and sodium increased oxygen extraction but decreased mesenteric vascular resistance while not affecting other parameters significantly. Since responses to prostacyclin did not coincide with responses to metabolically dependent transport of glucose and sodium, we conclude that the dilator metabolite of postprandial hyperemia is probably not prostacyclin.
D000818:Animals; D004285:Dogs; D004435:Eating; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D007421:Intestine, Small / Q000098:blood supply / Q000187:drug effects; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D011453:Prostaglandins / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects*; D013152:Splanchnic Circulation / Q000187:drug effects*
D011453:Prostaglandins; D011464:Epoprostenol