Kinetics of aggregation of human platelets.

A study of the aggregation kinetics of human platelets using an electronic counting device is reported. The experimental data were analyzed quantitatively by a physical model, which assumed that the initial disappearance rate of single platelets versus time fitted a second-order type of aggregation with respect to platelet number. The mechanism of aggregation was surface barrier controlled. Thus, the aggregation rate constants in different adenosine diphosphate concentrations (1.5-9.0 microgram) were 10-100 times greater than the rate constant (6.6325 x 10(-12) cm3/sec) for a diffusion-controlled mechanism, were smaller in the surface-barrier-controlled process and ranged from 0.00741 to 0.0467. The extent of aggregation was indicated by the calculation of a sticking probability constant as determined by the barrier. Adenosine diphosphate induced a rapid aggregating effect. Prostaglandin E1 produced the most drastic deaggregating effect as compared to dinoprostone (prostaglandin E2) and dinoprost (prostaglandin F2alpha). Aspirin completely blocked the aggregating effect of arachidonic acid.