Latency of pancreatic fluid secretory response to intestinal stimulants in the dog.

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Abstract
The effect of atropine and truncal vagotomy on the latency of the secretory response of the exocrine pancreas to rapid intraduodenal injection of L-tryptophan, sodium oleate and HCl or to rapid intraportal injection of secretin or CCK[cholecystohinin]-octapeptide was determined in conscious dogs with pancreatic fistulae. The intraduodenal stimulants were injected either alone or in the presence of an i.v. infusion of secretin, CCK-octapeptide or a combination of both hormones. The mean latency of response to tryptophan alone (62 .+-. 2 s), oleate alone (64 .+-. 5 s) and HCl alone (91 .+-. 3 s) was significantly longer (P < 0.05) than the latency to intraportal secretin (28 .+-. 5 s) or CCK-octapeptide (45 .+-. 4 s). Infusion of secretion alone or with CCK-octapeptide significantly shortened the latency of response to tryptophan (38 .+-. 3 s) and oleate (41 .+-. 5 s), but had no effect on the latency to intraduodenal HCl (96 .+-. 4 s). Atropine and truncal vagotomy both increased the latency to intraduodenal tryptophan and oleate 3-fold but did not affect the latency to intraduodenal HCl or intraportal secretin or CCK octapeptide. These data support the hypothesis that the stimulus to pancreatic fluid secretion evoked by intraduodenal HCl is humoral rather than neural, while the responses to intraduodenal tryptophan and oleate are mediated, at least in part, via an enteropancreatic, vagovagal, cholinergic reflex.

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