Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1991-12-27
pubmed:abstractText
A venous thrombosis model was produced by vessel wall damage generated by freezing a small segment of the rat jugular vein. The process of thrombus formation was investigated by electron microscopic study. Ultrastructural studies demonstrated that the initiation of thrombus formation could be deendothelialization caused by freezing of vessel. When blood flow was reestablished, platelets adhered to subendothelium within 1 min. Then platelets aggregated on the adhering platelets, and fibrin net was formed. Finally, thrombi composed predominantly of fibrin and red blood cells with platelet aggregates and leukocytes were generated. An anti-platelet agent, ticlopidine, revealed a potent antithrombotic effect in this model. Because ticlopidine decreased the number of platelet aggregates, reduced the size of aggregates, and inhibited platelet degranulation, it is conceivable that platelet aggregation in early phase of thrombus formation plays a crucial role even in venous thrombosis model. A synthetic thrombin inhibitor, argatroban, also showed a potent antithrombotic effect, but a thrombolytic agent, urokinase, was less effective. In conclusion, this model is both platelet- and coagulation-dependent.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0049-3848
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
373-84
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Effect of ticlopidine and other antithrombotics on the venous thrombosis induced by endothelial damage of jugular vein in rats.
pubmed:affiliation
Exploratory Research Laboratories 2, Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan.
pubmed:publicationType
Journal Article