Linked Life Data

8605016

Source:http://linkedlifedata.com/resource/pubmed/id/8605016

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-5-15
pubmed:abstractText
Reactive oxygen radicals have been implicated as mediators of anoxic injury in brain, but the cellular source of these radicals is unknown. In the periphery, there is evidence that endothelial cells play a fundamental role in anoxic tissue injury. The objective of the present study was to examine the response of rat brain endothelial cells to anoxia/reoxygenation injury in vitro. The results demonstrate that brain endothelial cells produce hydroxyl radicals and have increased nitric oxide synthase activity after anoxic injury. The increased production of nitric oxide in the cerebral endothelial cells does not appear to be mediated by an increase in either inducible or constitutive nitric oxide synthase. The radical trap alpha-phenyl-tert-butyl nitrone blocked hydroxyl free radical production, but not nitric oxide. These data suggest that the cerebral microcirculation may be an important site of oxygen free radical production in the brain in ischemic stroke.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
219
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
497-501
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Anoxic injury of endothelial cells increases production of nitric oxide and hydroxyl radicals.
pubmed:affiliation
Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't