Linked Life Data

9352611

Source:http://linkedlifedata.com/resource/pubmed/id/9352611

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-1-22
pubmed:abstractText
The vasodilator molecule nitric oxide is critically involved in the successful cardiopulmonary transition from fetal to postnatal life. It is produced in the pulmonary endothelium by the endothelial isoform of the enzyme nitric oxide synthase. The expression of endothelial nitric oxide synthase in the lung increases dramatically during late gestation, optimizing the capacity for nitric oxide production at the time of birth. Studies in cultured cell models indicate that the developmental upregulation may be mediated by estrogen, and that the expression of the enzyme is also upregulated by oxygen. Pulmonary endothelial nitric oxide synthase expression is diminished in models of congenital diaphragmatic hernia and neonatal pulmonary hypertension induced by fetal ductal ligation. Thus, there is normally a marked developmental upregulation in endothelial nitric oxide synthase expression in the lung during late fetal life, and attenuated expression of the enzyme may contribute to the pathophysiology of a variety of forms of neonatal pulmonary vascular disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0146-0005
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-92
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Ontogeny of nitric oxide in the pulmonary vasculature.
pubmed:affiliation
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235-9063, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't