AJP - Endocrinology and Metabolism, Vol 249, Issue 6 577-E583, Copyright © 1985 by American Physiological Society
Pentobarbital suppresses basal and reflexive pancreatic polypeptide release in dogs
G. J. Taborsky Jr, T. L. Paquette, M. A. Pfeifer and R. L. Gingerich
We sought to determine in overnight-fasted dogs whether basal or
2-deoxy-D-glucose (2-DG)-stimulated levels of pancreatic polypeptide (PP)
could be reliably used as an index of cholinergic activity at the pancreas
and thereby determine the effect of pentobarbital anesthesia on this
cholinergic outflow. At low basal PP levels, either atropine or
pentobarbital had a small effect on PP levels; at higher basal levels, both
atropine and pentobarbital had a larger effect. Thus both drugs decreased
PP in proportion to its initial basal level, suggesting that basal PP
levels have a variable cholinergic component. Atropine abolished the PP
response to intravenous 2-DG, confirming in our animal model that the PP
response to neuroglucopenia is entirely cholinergically mediated.
Pentobarbital also abolished the PP response to 2-DG, suggesting that
anesthesia either suppresses cholinergic outflow to the pancreas or the
response of the pancreatic F-cell to it. To test the latter hypothesis, the
acetylcholine analogue bethanechol was administered before and during
pentobarbital anesthesia. The PP response to direct cholinergic stimulation
was not abolished by pentobarbital, although it was reduced modestly. We
conclude that only part of the basal level of PP is under cholinergic
control; all of the PP response to 2-DG is cholinergically mediated;
pentobarbital anesthesia abolishes the cholinergic input to the pancreas;
and if the endogenous cholinergic input influences certain pancreatic
endocrine and exocrine responses, then its contribution would be seriously
underestimated when studied in pentobarbital-anesthetized animals.
