1991
DOI: 10.3109/00365529109003953
|View full text |Cite
|
Sign up to set email alerts
|

Pancreatic, Hepatic, and Duodenal Mucosal Bicarbonate Secretion during Infusion of Secretin and Cholecystokinin: Evidence of the Importance of Hepatic Bicarbonate in the Neutralization of Acid in the Duodenum of Anaesthetized Pigs

Abstract: The effect of infusion of secretin alone or in combination with cholecystokinin (CCK) on pancreatic, hepatic, and duodenal mucosal bicarbonate secretion was studied in anaesthetized pigs. After laparotomy, catheters were inserted into the common bile duct, the pancreatic duct, and both ends of the duodenum. Pancreatic, hepatic, and duodenal mucosal secretions were collected during intraportal infusion of increasing doses of secretin, either alone or in combination with CCK. During infusion of secretin in doses… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
4
0

Year Published

1992
1992
2018
2018

Publication Types

Select...
4
4

Relationship

2
6

Authors

Journals

citations
Cited by 12 publications
(4 citation statements)
references
References 27 publications
0
4
0
Order By: Relevance
“…27 Maximum bicarbonate concentration in humans may be as high as 150 mM, which is approximately twice as great as that in the rat. Sampling from the duodenum is fraught with hazards.…”
Section: Integrated Response Of Mealsmentioning
confidence: 99%
“…27 Maximum bicarbonate concentration in humans may be as high as 150 mM, which is approximately twice as great as that in the rat. Sampling from the duodenum is fraught with hazards.…”
Section: Integrated Response Of Mealsmentioning
confidence: 99%
“…As discussed in a review (Heitzmann and Warth 2007), it seems that the effect of CFTR on acid secretion may depend on the particular CFTR mutation and rescue by other Cl 2 transporters/channels. Normally, acid chyme is neutralized by HCO 3 2 secreted by duodenal epithelia, pancreatic duct and bile duct secretions (Ainsworth et al 1991). Therefore, duodenal hyperacidity in CF has been ascribed to loss-of-function in the CFTR transporter, especially in duodenal and pancreatic epithelia.…”
Section: How Does Hyperacidity Arise?mentioning
confidence: 99%
“…This, again, is supported by the fact that both hepatic and duodenal mucosal secretion of bicarbonate is stimulated by duodenal acidification (6,13) or by intravenous infusion of secretin or vasoactive intestinal peptide (VIP) (14)(15)(16), both of which are normally released to the blood stream by duodenal acidification. Furthermore, recent studies in our laboratory have shown that the secretion of bicarbonate from the porcine liver is greater than the secretion of bicarbonate from the pancreas during infusion of physiologic doses of secretin alone or in combination with cholecystokinin (CCK) (17). The purpose of the present study was to determine the relative importance of bicarbonate secretion from the liver, pancreas, and duodenal mucosa in neutralizing acid within the duodenal lumen.…”
mentioning
confidence: 97%