Linked Life Data

10806563

Source:http://linkedlifedata.com/resource/pubmed/id/10806563

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-7-6
pubmed:abstractText
Many studies failed to identify a hypercoagulable imbalance in the blood factors or decreased anticoagulant activity. On the other hand, fibrinolysis, a process unrelated to hypercoagulability but closely related to endothelial cell integrity, is predictably altered and contributes to the persistence of venous occlusion by thrombosis. There is considerable evidence that interruption of neurologic impulses and the ensuing paralysis cause metabolic changes in blood vessels and that blood vessel changes are accountable for venous thrombosis. Altered venous competence with complete spinal cord injury manifests by a decrease in venous distensibility and capacity and an increase in venous flow resistance. Vascular adaptations to inactivity and muscle atrophy, rather than the effect of a nonworking leg-muscle pump and sympathetic denervation, seem to lead to the thrombosis; indicating that thrombosis resulting from venous incompetence cannot be reversed by anticoagulation alone.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0889-8588
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
401-16
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Mechanisms of thrombosis in spinal cord injury.
pubmed:affiliation
Department of Medicine, Michigan State University, East Lansing, USA.
pubmed:publicationType
Journal Article, Review