Summary
Although elevated plasma epinephrine (epi) levels are associated with clinical atherothrombosis,
the role of epi in platelet-vessel wall interaction has not been established. Our
aim was to study the effect of high physiological epi (10 nM) in an experimental model
which tests the interaction between platelets and immobilized collagen in whole blood.
Shear forces and anticoagulation were modulated. Epi significantly enhanced platelet
deposition, but only at high shear rate (1,600 s-1)- In PPACK- or LMWH-anticoagulated blood, the increase in platelet deposition was
32 to 85 % (p <0.02-0.05). Furthermore, platelet aggregation was cotriggered with
subthreshold concentrations of epi and ristocetin, and monoclonal antibodies against
glycoprotein (GP) lb (AN 51 and SZ 2) attenuated epi-induced aggregation. We conclude
that epi is capable of augmenting platelet functions, which are dependent on the interaction
of vWF with GP lb and GP IIb/IIIa. Via this mechanism epi may promote arterial thrombosis
in vivo.
