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Vagal influence on exocrine pancreas of alcohol‐fed and of normal dogs
Author(s) -
SCHMIDT D. N.,
JOHNSON C. D.,
DEVAUX M.A.,
SARLES H.
Publication year - 1984
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1984.tb02098.x
Subject(s) - cholinergic , stimulation , endocrinology , medicine , pancreas , acetylcholine , chronic alcoholic , chemistry , alcohol , pancreatic juice , biochemistry
. A histochemical study has indicated increased activity of acetylcholine in the pancreas of chronic alcoholic dogs, and we have recently reported decreased pancreatic responsiveness to cholinergic stimulation in such dogs. This prompted us to determine, in chronic alcoholic dogs, the net pancreatic response to stimulation mediated by cholinergic nerves. Therefore, the pancreatic response to vagal stimulation by intravenous 2‐deoxy‐d‐glucose (2DG) infusion was examined in such dogs and in controls. After 2DG, 100 mg kg ‐1 , significant and similar increases in protein output up to maximally 2·7 ± 0·8 and 2·3 ± 0·5 mg kg ‐1 (15 min) ‐1 were observed in control and alcohol‐treated dogs. A significant rise in flow rate and HCO ‐ 3 output up to maximally 0·26 ± 0·07 ml kg ‐1 (15 min) ‐1 and 43 ± 13 μ mol kg ‐1 (15 min) ‐1 , respectively, occurred in the controls but was delayed in the alcoholics. The finding in alcoholic dogs of no change in protein response to 2DG is not in favour of a primary increase of vagally mediated pancreatic protein secretion. It could, however, be compatible with a primary increase in cholinergic receptor resistance due to alcohol and secondary adaptive increase in cholinergic activities, which when combined, would yield no net change of the cholinergically mediated protein response.