[Cholecystokinin incretion and the pharmacological effects on it in patients with chronic pancreatitis]

In patients with chronic pancreatitis (CP) (cholepancreatitis and primary recurrent pancreatitis), a moderate decrease of urocholecystokinin (UCK) excretion as a criterion for incretion of cholecystokinin-pancreozymin (CK) by duodenal endocrine cells was recorded in the presence of concomitant atrophic duodenitis. The beta-adrenoblocker obsidan, the blocker of m-cholinergic receptors gastrozepin, the antagonist of calcium channels finoptin and the synthetic analog of endogenous opiates dalargin reduced excretion of UCK in CP exacerbation. The decrease of CK incretion can be viewed as one of the mechanisms of the therapeutic action of these drugs in CP exacerbations. In the stage of CP remission, calcium gluconate consistently increased basal and intraduodenal oil (as a realizer of CK incretion) infusion-stimulated excretion of UCK. The enhancement of duodenal incretory activity is an essential mediating mechanism by which calcium gluconate stimulates pancreatic enzyme excretion.