Cardiopulmonary bypass leads to a preferential loss of activated platelets. A flow cytometric assay of platelet surface antigens.

OBJECTIVE

In a prospective study surface antigens associated with platelet activation, aggregation, and adhesion and the platelet volume were measured to investigate the mechanism of the platelet function defect of cardiopulmonary bypass (CPB).

METHODS

Blood samples were obtained during cardiac surgery before and after heparinization, as well as during and following extracorporeal circulation. The expression of the platelet surface glycoproteins (GP) IIb-IIIa, Ib, 53, and the granule membrane protein (GMP) 140 were measured using flow cytometry in platelet-rich plasma (PRP) before and after in vitro stimulation with adenosine diphosphate. A full blood count including mean platelet volume (MPV) was taken.

RESULTS

Heparinization resulted in a significant increase of GP 53 and GMP 140 and a significant decrease of GP Ib expression. During and following CPB, GP IIb-IIIa and Ib were significantly decreased. Similarly, the expression of the activation markers was reduced significantly. The mean platelet volume decreased significantly from 8.6 +/- 0.7 fl at baseline to 7.9 +/- 0.8 fl at the end of the study period.

CONCLUSION

Our data suggest that heparinization induces platelet activation. We assume that a loss of larger and more activated platelets from the circulation contributes substantially to the platelet function defect of CPB.