Linked Life Data

12031539

Source:http://linkedlifedata.com/resource/pubmed/id/12031539

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2002-5-28
pubmed:abstractText
Exposure to physical or psychological stress causes brain damage ranging from minimal behavioural alterations to neurodegeneration. One of the proposed mechanisms for stress-induced neurodegeneration is the overproduction of nitric oxide (NO) and related oxidative-nitrosative compounds via expression of the inducible NO synthase (iNOS). In the present investigation, the effect of acute or chronic immobilisation on blood-brain barrier (BBB) permeability and the possible role of iNOS were studied in adult male Wistar rats. Stress-induced [(14)C]-sucrose uptake by brain tissue correlates with the production of the stable NO metabolites nitrite and nitrate in both peripheral (plasma) and central (brain) compartments. Injection of the specific iNOS inhibitor 1400W (2 mg/kg, i.p.) prevents the stress-induced increase in BBB permeability. Taken together, these findings indicate that iNOS expression mediates stress-induced increase in BBB permeability and support a possible neuroprotective role for specific iNOS inhibitors in this situation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
938
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Stress-induced increase in extracellular sucrose space in rats is mediated by nitric oxide.
pubmed:affiliation
Departmento de Farmacología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't