Effect of 15(R), 15-methyl prostaglandin E2 and indomethacin on pancreatic secretion in man

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Abstract
In addition to gastric mucosal cytoprotective and antisecretory effects, prostaglandin E2 has a beneficial effect on experimental pancreatitis in some animal models, while prostaglandin synthesis inhibitors such as indomethacin and salicylates may induce pancreatitis at maximal doses. However, their effect on human pancreas is unclear. For this reason we considered it necessary to delineate their actions on human pancreatic secretion. Six healthy volunteers were studied on six separate days. On day 1, against a background of 1 pmol/kg/hr secretin, increasing doses of CCK were infused intravenously. On day 2, increasing doses of an amino acid mixture were infused intraduodenally and both studies were repeated on two occasions, following 100 μg 15(R), 15-methyl prostaglandin E2per os on one and following indomethacin 50 mg orally 12 and 1 hr prior to the study on the other. Both indomethacin and PGE2 had no significant effect on pancreatic secretion in response to graded doses of CCK. 15(R), 15-Methyl prostaglandin E2 and indomethacin caused a reduction of amylase output in response to the higher doses of intraduodenal amino acids. The prostaglandin E2 derivative also elicited a significant increase in basal bicarbonate output. In conclusion: the acute effects of 15(R), 15-methyl prostaglandin E2 and indomethacin on human pancreatic secretion do not seem to offer an explanation for the mechanisms of protection against experimental acute pancreatitis or an association with pancreatitis, respectively.