Shear Rate Dependence of Platelet Adhesion to Collagenous Surfaces in Willebrand Factor-Depleted Blood

A platelet function defect similar to that in von Willebrand’s disease, was produced by adding to human blood an antibody raised in rabbits against human factor Vlll/Willebrand factor. The effect of this antibody (F VIII Ab) on platelet adhesion was tested in an annular perfusion chamber. Only a small adhesion defect was observed at a shear rate corresponding to that in large arteries (830 s^-1) . Since bleeding usually occurs from small vessels, platelet adhesion to collagenous surfaces was investigated at higher shear rates corresponding to those in small vessels. The surfaces were exposed to human blood (l5mM citrate) at 1, 2 and 4x10³ s^-1 shear rate for 6, and 3 min, respectively. Different exposure times were chosen in order to obtain in control perfusions 50 – 70 % coverage of subendothelium with platelets at each shear rate. Platelet adhesion and adhesion-induced aggregation were measured morphometrically. As compared to control, F VIII Ab inhibited adhesion to subendothelium by 15±6, 32±21, 40±10 and 90±2 % (mean ± SE) at 0.83, 1, 2 and 4x10³ s^-1 shear rate, respectively. The corresponding inhibition by F VIII Ab observed on the fibrillar collagen of α-chymotrypsin-digested subendothelium was 62±11, 75±20, 99±1 and 100 %. In platelet rich plasma, F VIII Ab abolished Ristocetin-, inhibited collagen- and had no effect on ADP-induced aggregation.

Thus the defect in platelet adhesion to collagenous surfaces observed in Willebrand factor-depleted blood is minimal at low (venous) and maximal at high (small vessel) shear rates.