Linked Life Data

7453001

Source:http://linkedlifedata.com/resource/pubmed/id/7453001

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1981-3-17
pubmed:abstractText
Cholera toxin produces intestinal secretion and elevation of intestinal cyclic AMP. Nicotinic acid has been shown to prevent these responses. The effect of nicotinic acid on cholera toxin-induced secretion could be caused by decreased plasma-to-lumen flux, increased lumen-to-plasma flux, or a combination of both. The purpose of this study was to define the effects of nicotinic acid on net fluid movement and unidirectional sodium fluxes in rabbit jejunal loops exposed to cholera toxin. In the untreated animals receiving no nicotinic acid, the cholera toxin-exposed loops secreted 0.91 ml/cm/4h above the control loops receiving no cholera toxin (p < 0.01). On the other hand, pretreatment with 100 mg/kg nicotinic acid caused a striking decrease in secretion in the cholera toxin loop, so that the cholera toxin loop was not significantly different from the control loop. Unidirectional sodium fluxes in untreated animals showed that cholera toxin caused an increase in the plasma-to-lumen flux and a decrease in the lumen-to-plasma flux. Both effects were abolished by pretreating the animals with nicotinic acid. These studies indicate that nicotinic acid prevents cholera toxin-induced secretion by restoring the unidirectional fluxes to control levels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-7263
pubmed:author
pubmed:issnType
Print
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-11
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Effect of nicotinic acid on cholera-induced fluid movement and unidirectional sodium fluxes in rabbit jejunum.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't