Loss of fibrinogen receptors from the platelet surface during simulated extracorporeal circulation

In vitro recirculation of fresh human heparinized blood in an extracorporeal circuit with a membrane oxygenator decreased fibrinogen-induced platelet aggregation and diminished the number of fibrinogen receptors and glycoprotein IIb/IIIa (GPIIb/GPIIIa) antigenic sites on the platelet surface. In seven experiments, the mean ± SD K_m velue for fibrinogen (i.e., molar concentration of fibrinogen required to cause 50% of the maximal rate of aggregation) was 1.58 × 10^-7mol/L ± 0.68 × 10^-7 mol/L. After recirculation, this value increased to 3.8 × 10^-7 mol/L ± 1.94 × 10^-7 mol/L (P ≤ 0.025). The maximal aggregation rate of chymotrypsin-treated platelets decreased by 40% after 2 hours of recirculation (P ≤ 0.025). The number of fibrinogen receptors on platelets, which were treated with chymotrypsin after recirculation, decreased from 41,370 ± 24,000 to 13,230 ± 10,230/platelet under the same conditions (P ≤ 0.025). The number of antigenic sites for monoclonal antibody reacting with GPIIb/GPIIIa complex of adenosine diphosphate-stimulated platelets decreased from 34,200 ± 5,940 to 19,500 ± 9,680/platelet after recirculation (P ≤ 0.025). Prostaglandin E₁ (0.3 μmol/L) in the perfusion circuit preserved the ability of platelets to react with fibrinogen. In conclusion, the loss of fibrinogen receptors from the surface of platelet membranes results from the interaction of platelets with the surfaces of perfusion circuits.