Thromb Haemost 1983; 49(03): 196-198
DOI: 10.1055/s-0038-1657361
Original Article
Schattauer GmbH Stuttgart

Factors Influencing the Deaggregation of Chymotrypsin-Treated Human Platelets Aggregated by Fibrinogen

R L Kinlough-Rathbone
The Department of Pathology, McMaster University, Hamilton, Canada and the Department of Biochemistry, University of Toronto, Toronto, Canada
,
J F Mustard
The Department of Pathology, McMaster University, Hamilton, Canada and the Department of Biochemistry, University of Toronto, Toronto, Canada
,
M A Packham
The Department of Pathology, McMaster University, Hamilton, Canada and the Department of Biochemistry, University of Toronto, Toronto, Canada
,
E J Harfenist
The Department of Pathology, McMaster University, Hamilton, Canada and the Department of Biochemistry, University of Toronto, Toronto, Canada
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 09. März 1983

Accepted 24. März 1983

Publikationsdatum:
18. Juli 2018 (online)

Summary

Washed human platelets aggregated by ADP can be deaggregated by EDTA or PGE1; provided the release reaction does not occur; when the release reaction occurs platelets deaggregate less readily. Platelets treated with chymotrypsin are aggregated by fibrinogen indicating that fibrinogen receptors may be permanently exposed by this treatment. Fibrinogen-induced aggregation of chymotrypsin-treated platelets provides another method of bringing platelets into close contact with each other. Although EDTA deaggregated chymotrypsin-treated platelets aggregated by fibrinogen in a medium containing a physiological concentration of Ca2+, EDTA did not deaggregate these platelets if they were in a medium without calcium in which the release reaction occurs. In this medium, when ASA was added to prevent the release reaction, EDTA caused deaggregation. More fibrinogen associated with platelets in the medium without calcium than in the calcium-containing medium. In both media, EDTA displaced approximately half of the fibrinogen indicating that deaggregation is not solely dependent on dissociation of fibrinogen from its receptors. Thus when platelets undergo the release reaction, a form of platelet-to-platelet adhesion occurs that is not disrupted by chelation of divalent cations and is therefore not likely to involve only fibrinogen or thrombospondin and fibrinogen since the association of fibrinogen with its receptor requires Ca2+ and the binding of thrombospondin to platelets that have undergone the release reaction is also dependent on Ca2+.

 
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