Linked Life Data

7014260

Source:http://linkedlifedata.com/resource/pubmed/id/7014260

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1981-7-23
pubmed:abstractText
Hepatic metabolism of prostacyclin (PGI2) results in the formation of several biological inactive lipids and one product that has the chromatographic and biological properties of 6-keto-PGE1; the latter, unlike prostacyclin, is stable. Further, authentic 6-keto-PGE1, like PGI2, escapes pulmonary degradation and is a potent inhibitor of platelet aggregation. It could be generated from either prostacyclin or its inactive hydrolysis product 6-keto-PGF1 alpha via the 9-hydroxyprostaglandin dehydrogenase pathway, which has been identified in the liver and kidney. The prolonged biological activity of PGI2, which is difficult to explain in view of its inherent instability, may derive from transformation of PGI2 to 6-keto-PGE1. These studies raise the question: What, if any, of the effects of prostacyclin on platelets and the circulation are dependent on its conversion to 6-keto-PGE1?
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-9446
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2001-4
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Metabolism of prostacyclin: formation of an active metabolite in the liver.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't