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.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D001095:Arachidonic Acids / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D006403:Hematologic Tests; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D010974:Platelet Aggregation / Q000187:drug effects; D011458:Prostaglandins E / Q000494:pharmacology; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology
D001095:Arachidonic Acids; D011458:Prostaglandins E; D011459:Prostaglandins E, Synthetic; D011461:Prostaglandins F, Synthetic; D000244:Adenosine Diphosphate; D001241:Aspirin