Linked Life Data

10547097

Source:http://linkedlifedata.com/resource/pubmed/id/10547097

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1999-11-23
pubmed:abstractText
Accumulation of calcium following experimental traumatic brain injury (TBI) has been demonstrated to be a prominent pathophysiological component that can compromise mitochondrial functioning and threaten cell survival. The omega-conopeptide SNX-111, also known as Ziconotide, is a potent antagonist of the voltage-gated N-type calcium channel and has demonstrated significant neuroprotective effects against ischemia-induced neuronal injury. To determine whether this compound would be effective in reducing calcium accumulation associated with TBI, SNX-111 was administered intravenously to rats 1 hour following a moderate (2.2 to 2.75 atm) lateral fluid-percussion injury (or sham) at doses of 1 (n = 30), 3 (n = 31), or 5 (n = 30) mg/kg; another group received 0.9% saline solution (n = 35). Brains were processed for calcium 45 (45Ca) autoradiography at 6, 12, 24, 48, and 96 hours following insult. Optical density measurements of 20 cortical and subcortical regions were analyzed. Injured animals administered saline solution exhibited a significant increase in 45Ca uptake within 12 regions ipsilateral to the site of injury. The most prominent increases were evident throughout the ipsilateral cerebral cortex. SNX-111 reduced the injury-induced calcium accumulation within the ipsilateral cortex in a dose-response fashion when measured at 6, 12, and 48 hours after insult. These drug-induced reductions in calcium accumulation were as high as 75% in the ipsilateral cerebral cortex, and up to 50% in other ipsilateral regions (including thalamus and hippocampus). Consequently, the results suggest that posttraumatic blocking of the voltage-gated N-type calcium channel after injury reduces prolonged, trauma-induced calcium accumulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0897-7151
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
879-92
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10547097-Animals, pubmed-meshheading:10547097-Autoradiography, pubmed-meshheading:10547097-Brain, pubmed-meshheading:10547097-Brain Concussion, pubmed-meshheading:10547097-Brain Injuries, pubmed-meshheading:10547097-Calcium, pubmed-meshheading:10547097-Calcium Channel Blockers, pubmed-meshheading:10547097-Calcium Channels, N-Type, pubmed-meshheading:10547097-Calcium Radioisotopes, pubmed-meshheading:10547097-Cerebral Cortex, pubmed-meshheading:10547097-Functional Laterality, pubmed-meshheading:10547097-Hippocampus, pubmed-meshheading:10547097-Male, pubmed-meshheading:10547097-Neuroprotective Agents, pubmed-meshheading:10547097-Peptides, pubmed-meshheading:10547097-Rats, pubmed-meshheading:10547097-Rats, Sprague-Dawley, pubmed-meshheading:10547097-Thalamus, pubmed-meshheading:10547097-omega-Conotoxins
pubmed:year
1999
pubmed:articleTitle
Effects of an N-type calcium channel antagonist (SNX 111; Ziconotide) on calcium-45 accumulation following fluid-percussion injury.
pubmed:affiliation
Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095-7039, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't