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European Journal of Cardio-Thoracic Surgery, Vol 10, 768-773, Copyright © 1996 by European Association for Cardio-thoracic Surgery
A Wahba, G Black, M Koksch, G Rothe, J Preuner, G Schmitz and DE Birnbaum
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.
ARTICLES
Cardiopulmonary bypass leads to a preferential loss of activated platelets. A flow cytometric assay of platelet surface antigens
Department of Cardiae, Thoracic and Vascular Surgery, Klinikum Regensburg, University of Regensburg, Germany.
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