Further studies on prostaglandin E1-induced jejunal secretion of water and electrolytes in man, with special reference to the influence of ethacrynic acid, furosemide, and aspirin.

Perfusion studies were performed in 35 healthy volunteers to investigate further the secretory effect of prostaglandin E1 (PGE1), administered intraluminally, on the human jejunum. A perfusion system with a proximal occluding balloon and continuous aspiration of duodenal secretions was used. The influence of PGE1 (0.9 mug per kg per min) on glucose, fluid, and ion transport was entirely reproducible throughout a 6-hr perfusion experiment and was fully reversible 60 min after the end of PGE1 administration. The influence of ethacrynic acid (EA), aspirin (two agents previously reported to inhibit choleraic secretion), and furosemide was studied both on basal jejunal absorption and on PGE1-induced secretion of water and electrolytes. EA (2.5 mg per kg), administered in jejunal lumen, significantly reduced (P less than 0.001) the net secretory effect of intraluminal PGE1, and suppressed the PGE1-induced increase in plasma-to-lumen unidirectional flux of sodium. Intravenous or intraluminal aspirin (25 to 40 mg per kg) as well as intraluminal furosemide (1.5 mg per kg) did not modify the PGE1-induced secretion nor the basal absorption rates. Plasma immunoreactive levels of PGE1, calcitonin, and diverse gut hormones did not change significantly during PGE1-induced secretion. These results indicate that (1) aspirin, an inhibitor of prostaglandin synthesis, has no influence on the intestinal secretory effect of preformed PGE1; (2) EA, unlike furosemide, inhibits in man PGE1-induced jejunal secretion, an effect of EA similar to that observed in animals on cholera toxin- and cyclic AMP-mediated secretion.