The effect of partial exclusion of pancreatic juice from the intestine on the pancreatic response to intraduodenal infusion of casein, casein hydrolysate, and trypsin inhibitor was investigated in conscious rats with chronic pancreatic and biliary fistulas. In controls all pancreatic juice collected was returned to the intestine. In partial diversion groups only 10% of the pancreatic juice collected was returned during each collection period. All bile was returned. Partial diversion of pancreatic juice slightly increased the response to NaCl, had no effect on the incremental response to casein hydrolysate, but doubled the incremental protein and volume response to casein infusion. Trypsin inhibitor infusion did not stimulate pancreatic secretion in controls but greatly increased pancreatic protein and fluid secretion in rats with partial diversion of pancreatic juice. The results confirm that protein hydrolysates are weak stimulants of pancreatic secretion in the rat compared with intact proteins and support the view that intact proteins and trypsin inhibitors stimulate pancreatic secretion in the rat by a common mechanism, i.e., by reducing feedback inhibition from luminal pancreatic proteases.
The effect of atropine on the exocrine pancreatic secretory response to intestinally infused trypsin inhibitor and protein in conscious rats was investigated. Bile and pancreatic juice were collected and continuously returned to the intestine throughout all experiments. Ovomucoid trypsin inhibitor (OMTI) was infused at 1, 3, 6, 12, and 30 mg/h id, simultaneously with intravenously infused atropine (100 micrograms X kg-1 X h-1) or 0.15 M NaCl. Casein was infused at 300 mg/h id with or without intravenous atropine. Atropine inhibited basal pancreatic protein and fluid secretion 65.7 and 24.7%, respectively. Atropine had no effect on incremental (above basal) pancreatic protein and fluid output during infusion of maximally effective doses of OMTI (12 and 30 mg/h) and increased the incremental responses to submaximal doses of OMTI and to casein. The results are consistent with the hypothesis that cholecystokinin mediates negative feedback regulation by luminal proteases and that cholinergic mechanisms are not directly involved in this regulatory mechanism.
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