Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1984-11-28
pubmed:abstractText
Rats treated with subcutaneous 16,16-dimethyl prostaglandin E2 (16,16-dimethyl PGE2, 100 micrograms kg-1) exhibited diarrhoea even when their ileo-caecal junctions were tied, thereby eliminating contributions from small intestinal transit or fluid accumulation (enteropooling). The origin of the watery stool appeared to be the caecum, since tying the caecal-colonic junction eliminated it. The acceleration of colonic transit is likely to be a primary mechanism of PGE2-induced diarrhoea in the rat, since both normal animals and those with tied ileo-caecal junctions exhibited almost the same incidence of diarrhoea. Subcutaneous prostacyclin (PGI2) (2 mg kg-1 every 60 min) suppressed 16,16-dimethyl PGE2-induced diarrhoea in normal rats and in those with tied ileo-caecal junctions. Colonic transit measured in rats with cannula preimplanted in their proximal colon indicated that 16,16-dimethyl PGE2 enhanced colonic transit and PGI2 suppressed this increase. Thus, PGI2 can inhibit diarrhoea in the rat caused by 16,16-dimethyl PGE2 by suppressing colonic transit exclusive of its effects on small intestinal transit and enteropooling.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
157-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
The role of accelerated colonic transit in prostaglandin-induced diarrhoea and its inhibition by prostacyclin.
pubmed:publicationType
Journal Article