Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-10-24
pubmed:abstractText
The purpose of this study was to test the hypothesis that circulating ethanol at concentrations of approximately 0.1 mg% stimulates pancreatic secretion. Awake rats recovered from surgery were used in these experiments. Intravenous infusion protocols were established that produced blood ethanol concentrations 0.1 mg% for over an hour. Maintenance of 0.1 mg% blood ethanol concentration or transient concentrations as high as 0.17 mg% did not cause significant increases in pancreatic protein or fluid secretion. To test whether elevated blood ethanol would augment stimulated pancreatic secretion, the trypsin inhibitor camostat was infused intraduodenally at doses of 0.05, 0.2, and 0.5 mg/hr, each dose level infused for 2 hours. Elevated blood ethanol concentrations (0.1 mg%) did not significantly affect camostat-stimulated pancreatic protein or fluid secretion. In contrast to intravenous infusion, intraduodenal infusion of ethanol significantly stimulated pancreatic protein and fluid secretion, which was associated with blood ethanol concentrations of > or =0.19 mg%. The increases in pancreatic secretion were completely blocked by intravenous infusion of the cholecystokinin (CCK) receptor antagonist CR1409. We conclude that circulating ethanol does not stimulate pancreatic secretion in awake, recovered rats and that intraduodenal ethanol-stimulated pancreatic secretion is mediated by CCK.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1536-4828
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
e90-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Circulating ethanol does not stimulate pancreatic secretion in conscious rats.
pubmed:affiliation
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.