CHOLECYSTOKININ-8 INDUCES EDEMATOUS PANCREATITIS IN DOGS ASSOCIATED WITH SHORT BURST OF TRYPSINOGEN ACTIVATION

To study the early pathogenesis of acute edematous pancreatitis in dog s, we examined the relationship of pancreatic hyperstimulation with ch olecystokinin-8 (10 mu g/kg/hr intravenously for 6 hr) to alterations in circulating pancreatic enzymes and pancreatic morphology with speci al reference to trypsinogen activation. Cholecystokinin-8 infusion was associated with increases in plasma amylase, lipase, trypsin-like imm unoreactivity, and plasma and urine trypsinogen activation peptide. Pa ncreatic parenchymal swelling and interlobular and subcapsular fluid a ccumulations were detected ultrasonographically within 2 hr of cholecy stokinin-8. Circulating trypsin-like immunoreactivity and trypsinogen activation peptide in urine reached a peak at 2 and 4 hr, respectively , then declined despite progressive increases in circulating amylase a nd lipase and intrapancreatic fluid. No significant changes were obser ved in dogs receiving a saline infusion. This study illustrates that c holecystokinin-8 induces edematous pancreatitis in dogs that is associ ated with a short-lived burst of trypsinogen activation.