Atropine-Induced Inhibition of the Enhanced CCK Release Observed in Alcoholic Dogs

Abstract

As it has been previously shown, the pancreatic secretory response to an intraduodenal infusion of oleic acid is increased in animals accustomed to daily ethanol consumption compared to matched controls. This action has been verified in dogs provided with a Thomas cannula and consuming 2 g kg^-1 ethanol or not, daily since 3 years. An intravenous infusion of 0.75 mg kg^-1 h^-1 of atropine suppresses the difference between alcoholic and non-alcoholic animals. Therefore, the increased release of CCK-PZ in response to meal, which is characteristic of chronic alcoholic animals, is under cholinergic control.

Effects of Chronic Ethanol Consumption on Pancreatic Response to Central Vagal Stimulation by 2-Deoxy-<i>D</i>-Glucose in the Rat

“…This finding is emphasized by the results of Lechene de la Porte (personal commun.) showing modifications in the histological staining of cholinesterase and choline acetyl transferase in chronic alcoholic rats, and of Voirol et al (27) indicating that the enhanced protein excretion observed in alcoholic dogs after oleic acid is also atropine sensitive.…”

“…However animal models of chronic alcoholic pancreatic lesions have been only recently obtained (23), and many obscurities remain concerning the mechanism(s) by which chronic alcohol consumption may alter pancreatic function. The role of cholinergic mechanisms was recog nized long ago for the effects of acute alcohol (11) and was suggested more recently in various effects of chronic alcohol on the pancreas (15,(25)(26)(27). The aim of this paper is to describe some variations observed in response to pan creatic central vagal stimulation by 2-deoxy-/)-glucose (2DG) in rats drinking alcohol for 3 months.…”

Cholinergic Hypothesis of Alcoholic Pancreatitis

“…Cul ture of a human pancreatic cell line in the presence of pancreozymin induced a twofold increase in muscarinic receptor sites [43]. The augmentation of pancreatic sensitivity to pan creozymin induced by chronic alcohol admin istration is prevented by atropine [44], Simi larly, the effect of pancreozymin is poten tiated by raised intrapancreatic cholinergic tone [40], In vivo conditions seem to be essen tial for studying the effect of chronic alcohol intake on the response of pancreatic acinar cells to pancreozymin, since, although the hy perresponse to pancreozymin after chronic al cohol intake is well established in vivo, either a decreased, or a lack of response has been shown to occur in vitro [45][46][47],…”

Chronic Alcohol Consumption Does Not Modify Cholecystokinin Blood Levels Estimated by Bioassay in the Dog

“…If an increased cholinergic tone is partly responsible for this secretory pattern (8), changes in gastrointestinal hormone release also seem to play a role: secretin release being lower after intraduodenal HC1 (unpubl. data) and gastrin release higher after a meal (14) in alcoholic dogs than in controls.In previous papers it had been assumed that cholecystokinin (CCK) release was also increased because the percent increase from basal level of pancreatic protein output after intraduodenal oleic acid infusion was increased (7,15). In a more recent paper it was concluded that this was due to an experimental artefact (uncontrolled variations of basal secretion), pancreatic protein secretion after intraduodenal oleic acid (and therefore CCK release) being not modified by…”