Thromb Haemost 1984; 52(01): 057-059
DOI: 10.1055/s-0038-1661137
Original Article
Schattauer GmbH Stuttgart

Interactions of Purified Rat Factor VIII/von Willebrand Factor with Rat and Human Platelets – Effect of Albumin and Ristocetin[*]

E Dejana
1   The Istituto di Ricerche Farmacologiche “Mario Negri”, Milano, Italy
,
M Furlan
2   The Central Haematology Laboratory, Inselspital and University of Berne, School of Medicine, Berne, Switzerland
,
B Barbieri
1   The Istituto di Ricerche Farmacologiche “Mario Negri”, Milano, Italy
,
M B Donati
1   The Istituto di Ricerche Farmacologiche “Mario Negri”, Milano, Italy
,
E A Beck
2   The Central Haematology Laboratory, Inselspital and University of Berne, School of Medicine, Berne, Switzerland
› Author Affiliations
Further Information

Publication History

Received 25 July 1983

Accepted 18 May 1984

Publication Date:
19 July 2018 (online)

Summary

Rat platelets do not respond to ristocetin in their own plasma nor do they aggregate in the presence of bovine or porcine factor VIII von Willebrand factor (F VIII R:WF) or human F VIII R:WF in presence of ristocetin. However, rat plasma supports ristocetin induced aggregation of washed human platelets. In this study we report on purification of rat F VIII R:WF from cryoprecipitate. Similarly to porcine or bovine material, purified rat F VIII R:WF induced aggregation of human washed fixed platelets. This effect was enhanced by addition of ristocetin and was not modified by addition of albumin. Rat washed platelets were aggregated by ristocetin in the presence of rat or human F VIII R:WF provided that high concentrations of ristocetin are added in a system essentially free of extraneous proteins. Increasing concentrations of albumin dramatically reduced the ability of ristocetin to aggregate rat platelets while human platelet aggregation by human or rat F VIII R:WF was only moderately affected.

These studies show that rat F VIII R:WF can interact with rat and human platelets. The lack of response of rat platelets to ristocetin in their own plasma is most likely due to a low sensitivity of rat platelets to this drug and to an inhibitory activity of plasma proteins on this reaction.

*This work was supported by the Italian National Research Council (Progetto Finalizzato “Ingegneria genetica e basi molecolari delle malattie ereditarie” contratto n° 82.02384.51) and the Swiss National Science Foundation (n° 3.828-1.81).


 
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