Linked Life Data

1708485

Source:http://linkedlifedata.com/resource/pubmed/id/1708485

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1991-5-29
pubmed:abstractText
Hyperglycemia has been reported to alter outcome following experimental and clinical cerebral ischemia, but the mechanisms involved are incompletely understood. Since glucose influences the function of dihydropyridine-sensitive, voltage-gated Ca2+ channels in some non-neural cells, and since cellular Ca2+ overload has been implicated in the pathogenesis of ischemic neuronal injury, we examined whether glucose regulates Ca2+ channel function in a cultured neural cell line. Physiologic concentrations of glucose had no effect on free intracellular Ca2+ levels in PC12 cells, but 4-fold elevation of glucose above physiologic levels reduced the dihydropyridine-sensitive, depolarization-induced increase in Ca2+. This effect would not account for exacerbation of ischemic brain injury by hyperglycemia, but may contribute to attenuation of ischemic injury by glucose in certain settings.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
121
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
34-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Effects of glucose on calcium channels in neural cells.
pubmed:affiliation
Department of Neurology, University of California, San Francisco.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't