Linked Life Data

8896812

Source:http://linkedlifedata.com/resource/pubmed/id/8896812

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-2-18
pubmed:abstractText
Nitric oxide (NO) is considered to be associated with the pathogenesis of cerebral ischemic injury. In the present study, NO production was continuously monitored employing in vivo microdialysis. A microdialysis probe was inserted into the stratum. Levels of the major NO metabolite, NO-2, in the dialysate were determined using the Griess reaction. Rats were subjected to global cerebral ischemia produced by occlusion of both common carotid arteries together with induced hypotension. Cerebral ischemia induced a decrease in NO production, which was interrupted by a transient increase in NO synthesis. This increment was abolished in the presence of a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), suggesting that NO synthase activity is transiently activated during ischemia. Following reperfusion, NO synthesis was enhanced. To our knowledge, this is the first report concerning the continuous temporal profile of NO production during global cerebral ischemia and reperfusion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
734
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
86-90
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Brain nitrite production during global ischemia and reperfusion: an in vivo microdialysis study.
pubmed:affiliation
Department of Neurology, Keio University School of Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article