Linked Life Data

3896058

Source:http://linkedlifedata.com/resource/pubmed/id/3896058

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1985-8-30
pubmed:abstractText
Histopathological data obtained from different experimental models of hypoxia and ischemia were evaluated in order to extend current knowledge of mechanisms responsible for delayed neuronal cell death. Special attention is given to the distribution of calcium (Ca2+) in vulnerable areas during the postischemic period. Between an initial defensive Ca2+ sequestration, which is completely reversible, and final toxic Ca2+ overload, which is associated with irreversible neuronal necrosis, important Ca2+ shifts could be demonstrated cytochemically. Such shifts occur mainly at excitatory presynaptic sites and seem to precede structural ischemic cell change in postsynaptic areas. Recent results obtained with some Ca2+ entry blockers indicate that prophylactic treatment and postischemic intervention prevent cytosolic Ca2+ overload and reduce delayed brain injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0196-0644
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
736-42
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Ischemic brain injury and cell calcium: morphologic and therapeutic aspects.
pubmed:publicationType
Journal Article, Review