Male Wistar rats, fed a standard normal laboratory diet, drank ad libitum a 20% ethanol solution for 3 months. Basal and 2-deoxy-D-glucose (2DG) stimulated pancreatic secretion were measured. Basal secretion of sodium (-30%, p < 0.001), bicarbonate ( 35%, p < 0.001) and total protein ( 35%, p < 0.001) were depressed in alcoholic versus control rats. Pancreatic response was identical in both groups with the smaller dose of 2DG, dose related in controls, and identical for both doses in alcohol-fed rats. The response was thus significantly smaller in alcohol-fed rats than in controls for the larger dose of 2DG (p < 0.01). Pancreatic concentration and contents of amylase, trypsinogen, chymotrypsinogen and lipase were all decreased in alcoholic versus control rats (40–60%, p < 0.001). These results are consistent with the hypothesis of functional modifications in pancreatic cholinergic innervation in alcohol-fed rats.

Pancreatic secretion in anesthetized rats with acute fistulas was provoked by caerulein, acetylcholine, electrical stimulation of the vagus nerves or by 2-deoxy-D-glucose (2-DG). Venous infusions of norepinephrine, isoprenaline or dopamine inhibited the 2-DG-stimulated enzyme secretion but not that provoked by caerulein, acetylcholine or vagal electrical stimulation. Intracerebroventricular administration of norepinephrine or isoprenaline also inhibited 2-DG-stimulated enzyme secretion. It was confirmed that the amines stimulated water and electrolyte secretion by the pancreas in the order of potency isoprenaline > norepinephrine > dopamine. The results are consistent with a model whereby norepinephrine and isoprenaline exert their effect on pancreatic secretion via a central inhibition of vagal drive to the pancreas, together with a direct stimulating effect on water and electrolyte secretion at the level of pancreatic cells.

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