Linked Life Data

2168024

Source:http://linkedlifedata.com/resource/pubmed/id/2168024

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1990-10-2
pubmed:abstractText
Gray and white matter of the mammalian CNS are both damaged by anoxia. Anoxic injury in gray matter is mediated in part by excessive accumulation of excitotoxins like glutamate. Drugs such as ketamine, a dissociative anesthetic known to block glutamate (NMDA) receptors, reduce hypoxic neuronal injury in gray matter. In this study we used the isolated rat optic nerve preparation to determine if ketamine influences recovery after anoxia in a nonsynaptic system, ie, CNS white matter. Optic nerves from adult rats were exposed to a standard 60-minute period of anoxia. Ketamine (1 mM) improved recovery of the compound action potential (CAP) after anoxia. Since glutamate and aspartate (up to 10 mM) had no effect on CAP amplitude in the optic nerve, the effect of ketamine is probably not mediated by NMDA receptor blockade. These observations indicate that ketamine is able to protect CNS white matter, as well as gray matter, from anoxic injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0028-3878
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1399-403
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Anoxic injury of CNS white matter: protective effect of ketamine.
pubmed:affiliation
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't