Summary
Platelet adhesion to natural and artificial surfaces and adhesion-induced aggregation
were investigated in vitro using an annular perfusion chamber. The surfaces were exposed
to anticoagulated blood under identical flow conditions (~ arterial shear rates).
The initial attachment of platelets (contact) appeared less surface specific than
spreading and release. Fibrillar collagen was the most powerful inducer of platelet
degranulation whereas elastin, microfibrils and epon were virtually inactive. Fibrillar
collagen caused release also in the absence of spreading. Surface coverage with platelets
did not exceed 25 % unless spreading occurred. Perfusion with platelet-free plasma
or platelet-poor blood did not remove adhering platelets. However, platelets were
translocated from mural thrombi to the surface by such perfusion. In addition, platelets
which detached from mural thrombi adhered more readily to elastin or microfibrils
than platelets from the circulating blood. The initial attachment of platelets to
subendothelium was inhibited in von Willebrand’s disease, the Bernard-Soulier syndrome
and at high concentrations of dipyridamole; spreading was inhibited in storage pool
disease of rats, at low temperature (20° C), with EDTA (3 mM) and Prostaglandin E1 (1 μM); and adhesion-induced aggregation was inhibited in thrombasthenia, storage
pool disease and after ingestion of sulfinpyrazone or Aspirin.
It is concluded that the initial attachment (contact) of platelets, spreading and
surface-induced release of platelet constituents are at least partially independent
phenomena, the latter two being highly surface specific. At flow conditions which
cause the disappearance of platelet thrombi, platelet adhesion appears as an irreversible
process.
