Cardiopulmonary bypass leads to a preferential loss of activated plateletsA flow cytometric assay of platelet surface antigens

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Abstract
OBJECTIVE: In a prospective study surface antigens associated withplatelet activation, aggregation, and adhesion and the platelet volume weremeasured to investigate the mechanism of the platelet function defect ofcardiopulmonary bypass (CPB). METHODS: Blood samples were obtained duringcardiac surgery before and after heparinization, as well as during andfollowing extracorporeal circulation. The expression of the plateletsurface glycoproteins (GP) IIb-IIIa, Ib, 53, and the granule membraneprotein (GMP) 140 were measured using flow cytometry in platelet-richplasma (PRP) before and after in vitro stimulation with adenosinediphosphate. A full blood count including mean platelet volume (MPV) wastaken. RESULTS: Heparinization resulted in a significant increase of GP 53and GMP 140 and a significant decrease of GP Ib expression. During andfollowing CPB, GP IIb-IIIa and Ib were significantly decreased. Similarly,the expression of the activation markers was reduced significantly. Themean platelet volume decreased significantly from 8.6 +/- 0.7 fl atbaseline to 7.9 +/- 0.8 fl at the end of the study period. CONCLUSION: Ourdata suggest that heparinization induces platelet activation. We assumethat a loss of larger and more activated platelets from the circulationcontributes substantially to the platelet function defect of CPB.

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