Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1989-1-12
pubmed:abstractText
Antagonism of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors limits tissue damage after experimental cerebral ischemia. Spinal cord trauma leads to a progressive decline in blood flow that is associated with secondary tissue damage. In the present studies, we evaluated the hypothesis that NMDA receptor activation contributes to the pathophysiology of spinal cord injury by examining the effects of the NMDA antagonist MK801 after impact trauma to rat thoracic spinal cords. MK801, in doses of 1.0 and 5.0 mg/kg administered intravenously (IV) at 15 min after trauma, improved long-term neurologic recovery. At a dose of 1.0 mg/kg, the drug reduced histologic changes as well as alterations in certain tissue cations found after spinal trauma. These findings suggest that excitotoxins contribute to the pathophysiology of spinal cord injury and that early treatment with NMDA antagonists may reduce posttraumatic tissue damage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0897-7151
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-45
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
N-methyl-D-aspartate antagonist MK801 improves outcome following traumatic spinal cord injury in rats: behavioral, anatomic, and neurochemical studies.
pubmed:affiliation
Department of Neurology, University of California, San Francisco.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.