Effect of vagotomy and/or antrectomy on gastric secretion stimulated by intravenous infusion of bethanechol chloride

1971 ◽  
Vol 16 (1) ◽  
pp. 19-26 ◽  
Author(s):  
K. Kowalewski
1982 ◽  
Vol 242 (6) ◽  
pp. G603-G607
Author(s):  
A. Sonnenberg ◽  
S. A. Muller-Lissner ◽  
G. Schattenmann ◽  
J. R. Siewert ◽  
A. L. Blum

Duodenogastric reflux, gastric emptying, and gastric secretion were measured simultaneously by a double-marker technique after instillation of a liquid lipid meal (300 ml Intralipid) or a protein meal (300 ml Bactopeptone) in five trained mongrel dogs. A lipid meal was emptied slower and elicited less volume secretion than a protein meal. Duodenogastric reflux rate and intragastric accumulation of duodenal contents were similar with both meals. Intravenous infusion of atropine slowed gastric emptying and inhibited gastric volume secretion only in the case of protein meal. Atropine increased duodenogastric reflux rate and gastric accumulation of duodenal contents with both protein and lipid meals. The percentage of duodenal contents inside the stomach increased continuously during gastric emptying; it did not exceed 20% with both meals given alone and 40% with both meals given together with atropine. It is concluded that duodenogastric reflux and gastric accumulation of duodenal contents are common phenomena during gastric digestion of a meal. The degree of such accumulation does not depend on the type of meal. Intragastric accumulation of duodenal contents is increased when duodenogastric reflux rate is stimulated and when gastric emptying rate is inhibited simultaneously.


1959 ◽  
Vol 197 (2) ◽  
pp. 253-256 ◽  
Author(s):  
Marjorie K. Lavers ◽  
Patricia A. Stefanik ◽  
Charles F. Code

A study was undertaken to determine the effect of thiamine deficiency on the hydrochloric acid output of vagally denervated gastric pouches (Heidenhain-type) and vagally innervated gastric pouches (Pavlov-type) in dogs. Responses of both types of pouches to injection of 0.05 mg of histamine/kg of body weight and the maximal secretory capacity of both types after histamine were unaltered during the deficiency state. A degree of thiamine deficiency sufficient to produce anorexia and neuritis was without effect on the secretory response of canine gastric mucosa to histamine. The hydrochloric acid output of vagally innervated pouches during nervous stimulation caused by insulin-induced hypoglycemia was drastically reduced as soon as thiamine deficiency developed, while the response to bethanechol chloride was little, if at all, affected. It is concluded that the vagal secretory mechanism participates in the general neural failure of thiamine deficiency and that this failure most likely is in the neurons of the vagal nuclei.


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