Linked Life Data

10832406

Source:http://linkedlifedata.com/resource/pubmed/id/10832406

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-8-3
pubmed:abstractText
Nitric oxide (NO), an intercellular messenger and a normal metabolic product, takes an active part in the regulation of physiologically significant functions of the cardiovascular, immune, and nervous systems. At the same time when produced in excess amounts, NO as a free radical and an agent that gives rise to highly toxic oxidants (peroxynitrile, nitric dioxide, nitron ion), becomes a cause of neuronal damage and death in some brain lesions (parkinsonism, Alzheimer's disease, Huntington's chorea). Numerous experimental data show the ambiguous effects of NO on the development of cerebral infarct. NO as an active vasodilatory and antithrombogenic agent may reduce cerebral damage in early ischemia. There is evidence for the involvement of NO in the body's adaptation to oxygen starvation and ischemic tolerance formation. In the postischemic period, NO is a major factor of neuronal necrosis and apoptosis. The currently established ideas on the processes of cerebral NO production and on the pathogenetic mechanisms of this agent's cytotoxicity open up new vistas for selective blockers of various NO synthesis enzymes (neuronal, endothelial, glial cellular, and macrophagal and neutrophilic NO synthases) used in the treatment of acute vascular abnormalities of the central nervous system.
pubmed:language
rus
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0869-6047
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5-10
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
[The role of nitric oxide and other free radicals in ischemic brain pathology].
pubmed:publicationType
Journal Article, English Abstract, Review