Linked Life Data

8773794

Source:http://linkedlifedata.com/resource/pubmed/id/8773794

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1996-11-25
pubmed:abstractText
Previous studies have implicated both excitotoxicity and apoptosis in the pathogenesis of cerebral infarction induced by focal ischemic insults. Here we tested the possibility that the NMDA antagonist, dextrorphan, and the protein synthesis inhibitor, cycloheximide, would produce additive protective effects in a rodent model of focal ischemia-reperfusion. Transient focal cerebral ischemia was induced by a 90 min period of ligation of the right middle cerebral artery and both common carotid arteries. Administration of either 30 mg/kg dextrorphan or 0.5 mg/kg cycloheximide, given i.p. 15 min before ischemia, reduced infarct volume by about 65%. When optimal concentrations of each drug were given together, infarct volume was reduced by 87% as measured 14 days later. These observations support the idea that both excitotoxicity, and apoptosis dependent on new protein synthesis, contribute to cerebral infarction after transient focal ischemia in the rat.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
718
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-6
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Additive neuroprotective effects of dextrorphan and cycloheximide in rats subjected to transient focal cerebral ischemia.
pubmed:affiliation
Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
pubmed:publicationType
Journal Article