Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-6-16
pubmed:abstractText
Nalmefene is an opiate receptor antagonist, derived from naltrexone, that has a significantly longer plasma half-life than naloxone after i.v. administration and that may have enhanced activity at kappa opiate receptors. Because of the demonstrated beneficial effects of other opiate-receptor antagonists in spinal cord injury (SCI) and the postulated role of kappa opiate receptors in such injury, nalmefene treatment was evaluated in a well-characterized model of traumatic SCI in rats. In a randomized blinded study, nalmefene treatment, given as a single i.v. bolus injection at 60 min posttrauma, significantly improved neurological recovery and reduced tissue damage. Beneficial actions were dose-related. The optimal dose was 0.1 mg/kg, with diminished effects at both higher and lower doses; this is approximately 1% of the optimal naloxone dose in SCI as shown from other studies. Nalmefene, given i.t. at doses that were ineffective systemically, significantly improved neurological recovery after spinal trauma. These findings are consistent with the hypothesis that endogenous opioids, acting at opiate receptors within the spinal cord, mediate certain secondary pathophysiological changes that contribute to irreversible tissue injury. If current clinical trials with naloxone in SCI prove successful, the profile of nalmefene would make it a candidate for use in future clinical studies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
245
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
742-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Opiate-receptor antagonist nalmefene improves neurological recovery after traumatic spinal cord injury in rats through a central mechanism.
pubmed:affiliation
Department of Neurology, University of California, San Francisco.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.