Linked Life Data

8774797

Source:http://linkedlifedata.com/resource/pubmed/id/8774797

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-11-19
pubmed:abstractText
The endothelial cell (EC) was once though to be a passive bystander in the inflammatory response to shock and injury. We now know, however, that these cells play a central role in the coordination of the response to injury. Hypovolemic shock following traumatic injury initiates two primary mechanisms of cellular damage. These include ischemia/reperfusion injury and acute inflammation. The EC has four key functions that are altered by these states: a) control of coagulation, b) regulation of vascular tone, c) control of vascular permeability, and d) regulation of leukocyte adhesion and trafficking. In the settings of ischemia/reperfusion and acute inflammation, the EC takes on a proinflammatory phenotype and as such becomes prothrombotic, demonstrates enhanced vascular permeability, and becomes chemoattractant, facilitating leukocyte adhesion, activation, and migration. In this article, we explore each of the four EC functions in detail along with the alterations that occur when the proinflammatory phenotype becomes manifest. In addition, we elucidate novel therapeutic strategies that have arisen from this research.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1063-7389
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
211-23
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Endothelial changes after shock and injury.
pubmed:affiliation
Department of Surgery, Harborview Medical Center, University of Washington, Seattle 98104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review