POTENTIATION OF CANINE PANCREATIC BICARBONATE OUTPUT BY OLEIC-ACID ISNOT NEURALLY DEPENDENT

To study neural involvement in potentiation of acid-induced pancreatic bicarbonate output, six dogs underwent extrapancreatic denervation an d pancreatic fistula creation. Pancreatic responses to secretin (16 an d 32 ng/kg/h) and cholecystokinin (50 ng/kg/h) were then assessed. The duodenum was then perfused with three sets of perfusates. The first s et contained hydrochloric acid with either D- or L-phenylalanine, The second set contained bovine serum albumin and hydrochloric acid with o r without oleic acid; the albumin and acid were varied so that each 50 ml contained 1, 2, or 4 meq titratable acid (pH 2.0-4.5). The third s et was identical to the second except for initial pH of 3.5. Pancreati c responses predicted upon addition of cholecystokinin to secretin, L- phenylalanine to hydrochloric acid, or oleic acid to bovine serum albu min were compared with observed responses. At both doses, secretin-ind uced bicarbonate output was increased by cholecystokinin (16 ng/kg/h: 0.88 +/- 0.29 meq/15 min; 32 ng/kg/h: 1.01 +/- 0.23 meq/15 min). The l atter significantly exceeded predicted output (16 ng/kg/h: 0.38 +/- 0. 10 meq/15 min; 32 ng/kg/h: 0.58 +/- 0.15 meq/15 min), verifying potent iation. L-phenylalanine failed to potentiate bicarbonate output evoked by acidified D-phenylalanine. In contrast, addition of oleic acid to pH 2.0 or 3.5 bovine serum albumin potentiated bicarbonate output. The se data suggest that enteropancreatic reflexes mediate potentiation of acid-induced pancreatic bicarbonate output by amino acids, but not by fatty acids.