Linked Life Data

12405032

Source:http://linkedlifedata.com/resource/pubmed/id/12405032

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
40
pubmed:dateCreated
2002-10-30
pubmed:abstractText
Ischemic tolerance means a rapid adaptative cerebral reaction to one or more cycles of short ischemia and reperfusion, improving the tolerance to a subsequent longer ischemia. The basic molecular mechanisms of ischemic tolerance are largely unknown. The pathophysiological course can be divided in induction, transduction and tolerance. During induction NMDA- and adenosin receptors, free radicals and conservation of energy metabolism are required. Protein kinases, transcription factors, and immediate early genes play a role in transduction. Tolerance can be observed in different time windows. The early phase lasts for several hours after the preconditioning stimulus and can be related to adenosine receptors and ATP-dependent potassium channels. A delayed phase, after 1-7 days, is explained by genetic remodeling. Clinically, there is evidence for a protective effect of transient ischemic attacks occurring before stroke.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1661-8157
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1639-44
pubmed:dateRevised
2008-6-10
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
[Cerebral ischemia tolerance].
pubmed:affiliation
Max-Planck-Institut für Neurologische Forschung, Köln. Bernhard.Schaller@pet.mpin-koeln.mpg.de
pubmed:publicationType
Journal Article, English Abstract, Review