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

• Published in: European journal of cardio-thoracic surgery 1996-09, Vol.10 (9), p.768-773
• Main Authors: WAHBA, A, BLACK, G, KOKSCH, M, ROTHE, G, PREUNER, J, SCHMITZ, G, BIRNBAUM, D. E
• Format: Article
• Language: English
• Subjects: Adult; Aged; Anesthesia; Anesthesia depending on type of surgery; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Anticoagulants - adverse effects; Antigens, CD - metabolism; Biological and medical sciences; Blood Platelet Disorders - etiology; Blood Platelet Disorders - immunology; Blood Platelet Disorders - metabolism; Cardiopulmonary Bypass - adverse effects; Flow Cytometry; Glycoproteins - metabolism; Heparin - adverse effects; Humans; Medical sciences; Middle Aged; Platelet Activation; Platelet Function Tests; Platelet Glycoprotein GPIb-IX Complex - metabolism; Platelet Glycoprotein GPIIb-IIIa Complex - metabolism; Platelet Membrane Glycoproteins - metabolism; Prospective Studies; Tetraspanin 30; Thoracic and cardiovascular surgery. Cardiopulmonary bypass
• ISSN: 1010-7940; 1873-734X
• DOI: 10.1016/S1010-7940(96)80338-1

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.