Role of platelet glycoprotein IIb/IIIa in ADP-activated platelet adhesion to aortic endothelial cells in vitro: observation with video-enhanced contrast microscopy

Intravascular thrombus formation downstream of cerebral arterial occlusion may result in necrosis of ischemic tissue. To clarify the causative mechani sms, interaction between adenosine-5'-diphosphate (ADP)-activated platelets and cultured human aortic endothelial cells (HAEC) was examined by employi ng video enhanced contrast-differential interference contrast (VEC-DIC) mic roscopy. The numbers of (1) control/platelets, (2) ADP-activated platelets, (3) ADP-activated, anti-platelet GP Iba antibody (GUR20-5)-treated platele ts, and (4) ADP-activated, platelet GP IIb/IIIa antagonist (TAK-MB)-treated platelets, associated with HAEC after superfusion and wash-out were counte d in visual fields of 30 x 30 mum(2). Many ADP-activated platelets adhered to HAEC directly, while almost no platelets adhered to HAEC in the control. The adhesion was almost completely blocked by the GP IIb/IIIa antagonist, but not by GP lb(x antibody. We conclude that initial binding of ADP-activa ted platelets to HAEC is mediated by platelet GP IIb/lIIa in this in vitro system.