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+.
Keywords
Platelets - Deaggregation - Chymotrypsin - Fibrinogen - Release reaction - Aspirin