Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2007-9-21
pubmed:abstractText
Inflammation and microvascular dysfunction have been implicated in a variety of pathologic conditions affecting the brain. Features of the inflammatory response that are common to many of these pathological conditions and that are manifested in the neurovasculature include oxidative stress, diminished endothelial barrier function (increased vascular permeability), increased expression of endothelial cell adhesion molecules, and the recruitment of rolling and adherent leukocytes and platelets. The evidence implicating leukocyte-endothelial cell adhesion in cerebral microvessels as a rate-determining component of the pathophysiology associated with conditions such as ischemia-reperfusion, sickle cell disease, and gamma -irradiation is summarized. Mechanisms that have been proposed to explain the recruitment of adherent leukocytes and platelets in the diseased/injured cerebral microvasculature are also addressed, and a common paradigm for blood cell recruitment induced by seemingly unrelated pathological conditions is outlined. Although there are many structural and functional characteristics of the cerebral microvasculature that distinguish it from other regional vascular beds, the processes that underlie the recruitment of injury-causing inflammatory cells in the brain appear to closely resemble those described for other tissues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1073-9688
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
667-81
pubmed:meshHeading
pubmed:articleTitle
The evolving paradigm for blood cell-endothelial cell interactions in the cerebral microcirculation.
pubmed:affiliation
Centre for Biochemical Pharmacology, William Harvey Research Institute, London, UK.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural