Platelet adhesion to damaged coronary arteries: Comparison in normal and von Willebrand disease swine.
AUTOR(ES)
Reddick, R L
RESUMO
The early response to coronary artery injury was investigated in normal swine and in swine with von Willebrand disease (vWD). Thirty minutes after coronary endothelial denudation, a monolayer of platelets was adherent to areas of simple injury in both bleeder and normal swine. The number of adherent platelets was not significantly different in the two phenotypes. Injury involving the media of the vessel produced platelet-fibrin thrombi. Platelet activation, as judged by pseudopod formation and platelet spreading over areas of simple injury, was significantly less in bleeder animals than in normal animals. These studies suggest that chemotaxis and initial contact adhesion of platelets to injured arterial wall is independent of the von Willebrand factor. On the other hand, the spreading and activation of platelets on the subendothelium appear to be dependent on the presence of plasma von Willebrand factor. Through this mechanism von Willebrand factor may contribute to arterial thrombosis and atherogenesis.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=346830Documentos Relacionados
- von Willebrand's disease antigen II. A new plasma and platelet antigen deficient in severe von Willebrand's disease.
- Platelet interaction with rabbit subendothelium in von Willebrand's disease: altered thrombus formation distinct from defective platelet adhesion.
- von Willebrand factor mediates platelet adhesion to virally infected endothelial cells.
- von Willebrand factor binds to platelets and induces aggregation in platelet-type but not type IIB von Willebrand disease.
- Aortic stenosis and angina with normal coronary arteries: the role of coronary flow abnormalities.