Linked Life Data

10378318

Source:http://linkedlifedata.com/resource/pubmed/id/10378318

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-4
pubmed:dateCreated
1999-8-19
pubmed:abstractText
Deep venous thrombosis is initiated primarily in the pockets of the valves of the veins of the lower limbs and the main pelvic veins. In addition to a genetic predisposition there are several acquired conditions associated with deep venous thrombosis such as major surgery, trauma, cancer, pregnancy, and immobilization. While major diseases as well as hormonal changes have been shown to cause changes in blood coagulation and fibrinolytic factors, the impact of immobilization per se is much less clear. It has been shown that in the absence of intermittent pulsatile flow the blood within the valve pockets became rapidly hypoxic when undisturbed during streamline flow (i.e. when "static"). Hypoxia on the other hand has been shown to cause procoagulatory changes of the vascular endothelium (e.g. production of platelet activating factor [PAF], expression of tissue factor), adhesion and activation of leukocytes and expression of tissue factor on their surface, as well as the activation of platelets. Together with reduced removal and/or inactivation of active clotting factors these mechanisms might contribute to the development of deep venous thrombosis during immobilization.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0043-5341
pubmed:author
pubmed:issnType
Print
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
[Pathophysiology of immobilization].
pubmed:affiliation
Institut für Gefässbiologie und Thromboseforschung, Universität Wien. margarethe.geiger@univie.ac.at
pubmed:publicationType
Journal Article, English Abstract