Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1990-3-30
pubmed:abstractText
Both N-methyl-D-aspartate (NMDA)-receptor antagonists and opiate-receptor antagonists have been shown to limit tissue damage after ischemic central nervous system injury. We compared the neuroprotective effects of the noncompetitive NMDA-receptor antagonist MK-801 and the opiate-receptor antagonist nalmefene in a model of global spinal cord ischemia and reperfusion in unanesthetized rabbits. MK-801 (1 mg/kg) or nalmefene (0.1 mg/kg) was administered intravenously 5 minutes after reperfusion. MK-801 treatment and nalmefene treatment each significantly improved the neurologic and histologic outcome compared with saline controls. Differences in these outcome measures between MK-801 treatment and nalmefene treatment did not reach statistical significance. Our results are consistent with the hypothesis that multiple factors, including endogenous opioids and excitatory amino acids, contribute to the secondary tissue injury after central nervous system ischemia. These data also provide further evidence that therapeutic interventions with opiate-receptor antagonists or NMDA antagonists may be beneficial in limiting neurologic dysfunction after ischemic brain or spinal cord injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0003-9942
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
277-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Comparison of the neuroprotective effects of the N-methyl-D-aspartate antagonist MK-801 and the opiate-receptor antagonist nalmefene in experimental spinal cord ischemia.
pubmed:affiliation
Department of Neurology, University of California, San Francisco.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S.