Linked Life Data

10773646

Source:http://linkedlifedata.com/resource/pubmed/id/10773646

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-6-30
pubmed:abstractText
The potential role of inflammatory mechanisms in the pathophysiology of ischemic brain damage has intensely been discussed. We have recently demonstrated that stroke patients display an intrathecal production of proinflammatory cytokines early after onset of symptoms. IL-1beta, one of these cytokines, stimulates the production of nitric oxide (NO), a potent inflammatory mediator. The aim of the present study was to investigate the intrathecal levels of nitrate, one of the main metabolites of NO in acute stroke and to relate its levels to brain damage. Stroke patients were prospectively studied with clinical evaluation, radiological assessment and analysis of intrathecal levels of nitrate by gas chromatography/mass spectrometry. In addition, simultaneous analyses of cytokines and of soluble Fas/APO-1 and bcl-2, two proteins regulating apoptosis, were performed. The intrathecal levels of nitrate were not significantly different in stroke patients compared to controls throughout the observation period. However, the intrathecal levels of nitrate increased significantly 3 months after stroke onset compared with the first 3 days. Interestingly, the levels of nitrate measured at stroke onset were negatively correlated to the final size of infarct volume (r = -0.69, p < 0.05) measured by MRI. In addition, patients with large infarcts displayed significantly (p = 0.008) lower levels of nitrate in cerebrospinal fluid compared to patients with small infarcts during the first 3 days after stroke onset. In contrast, the intrathecal levels of nitrate were significantly positively correlated (r = 0.79, p < 0. 001) to the neurological deficit and negatively correlated (r = -0. 76, p < 0.05) to bcl-2, a protein downregulating neuronal apoptosis, in the late stage of the stroke. Early NO production is associated with a smaller infarct volume, suggesting a protective effect, whereas late NO production is associated with severer neurological deficits, suggesting a neurotoxic effect. Treatment trials pertaining to modulate NO production in stroke should take into consideration the dual effect of NO on ischemic brain damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1015-9770
pubmed:author
pubmed:copyrightInfo
Copyright 2000 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
200-6
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10773646-Adult, pubmed-meshheading:10773646-Aged, pubmed-meshheading:10773646-Antigens, CD95, pubmed-meshheading:10773646-Apoptosis, pubmed-meshheading:10773646-Biological Markers, pubmed-meshheading:10773646-Brain, pubmed-meshheading:10773646-Brain Damage, Chronic, pubmed-meshheading:10773646-Cytokines, pubmed-meshheading:10773646-Female, pubmed-meshheading:10773646-Gas Chromatography-Mass Spectrometry, pubmed-meshheading:10773646-Humans, pubmed-meshheading:10773646-Magnetic Resonance Imaging, pubmed-meshheading:10773646-Male, pubmed-meshheading:10773646-Middle Aged, pubmed-meshheading:10773646-Nitrates, pubmed-meshheading:10773646-Nitric Oxide, pubmed-meshheading:10773646-Reference Values, pubmed-meshheading:10773646-Stroke, pubmed-meshheading:10773646-Time Factors, pubmed-meshheading:10773646-Tomography, X-Ray Computed
pubmed:articleTitle
Intrathecal release of nitric oxide and its relation to final brain damage in patients with stroke.
pubmed:affiliation
Department of Rheumatology, University of Göteborg, Sweden. andrej.tarkowski@microbio.gu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't