Anti-glycoprotein Ib causes platelet aggregation

Abstract

In 1987 we reported that when blood was forced through a fine filter under pressure in the filterometer the platelets aggregated and blocked the filter. von Willebrand factor (vWF) and glycoprotein (Gp) IIb/IIIa and calcium were involved. Results with anti-GpIb were equivocal. We now report that all the anti-GpIb antibodies studied, glycocalicin, as well as some concentrations of aurin tricarboxylic acid caused platelet aggregation in the pre-filter blood and therefore could not be used in the filterometer. Using two different molecules that prevent vWF binding to GpIb and two anti-GpIIb/IIIa antibodies at two pressures it has now been shown that GpIb, vWf and high shear are primarily responsible for platelet retention at 0-5 s. Progressive platelet retention studied between 20 and 40 s required high shear and GpIIb/IIIa after the calcium influx mediated by GpIb/vWF binding. When GpIb was inhibited, GpIIb/Ila could not function normally, so GpIb inhibition resulted in decreased aggregation both at 0-5 s and at 20-40 s. Anti-GpIIlb/IIIa caused a minimal decrease in retention at 0-5 s and marked inhibition at 20-40 s. These findings fit and amplify concepts derived from other high shear methodologies. A diagram is presented of the events leading up to the final 'passivation' of the 'thrombus' in the filter when the surface of the aggregated platelets becomes unattractive.