Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-12-4
pubmed:abstractText
The vascular endothelium plays a critical role in the regulation of coagulation through the constitutive expression and release of anticoagulants and the inducible expression of procoagulant substances. Cardiopulmonary bypass dysregulates this process by activating endothelial cells, initially promoting bleeding and then thrombosis. Endothelial cell activation in response to circulating inflammatory mediators leads to the initiation of coagulation when tissue factor is expressed throughout the intravascular space. This results in the widespread consumption of coagulation factors. Additionally, there is a cardiopulmonary bypass-related qualitative platelet defect that is exacerbated by thrombocytopenia as platelets are consumed from the circulation by clot and adherence to the cardiopulmonary bypass circuit. Finally, cardiopulmonary bypass results in the endothelial release of plasminogen activators, which lead to an increase in systemic fibrinolysis. The diffuse generation of thrombin, driven by the inducible intravascular expression of tissue factor, plays a major role in all of these processes. Efforts to understand the critical role of the endothelium in coagulation may lead to novel therapies to prevent bleeding or thrombosis in cardiovascular surgery patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0003-4975
pubmed:author
pubmed:issnType
Print
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1549-57
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Endothelial cell injury in cardiovascular surgery: the procoagulant response.
pubmed:affiliation
Division of Cardiothoracic Surgery, University of Washington, Seattle 98195, USA.
pubmed:publicationType
Journal Article, Review