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J Thorac Cardiovasc Surg 1998;115:1160-1165
© 1998 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

Disappearance of glycoprotein Ib from the platelet surface in pericardial blood during cardiopulmonary bypass

From the Department of Cardiopulmonary Surgery, Onze Lieve Vrouwe Gasthuis, Amsterdam,^a and the Department of Clinical Chemistry, Leiden University Medical Center, Leiden,^b The Netherlands.

Received for publication July 22, 1997. Revisions requested Sept. 2, 1997; revisions received Oct. 30, 1997. Accepted for publication Nov. 14, 1997. Address for reprints, K. N. Maquelin, MD, Onze Lieve Vrouwe Gasthuis, Department of Cardiopulmonary Surgery, P.O. Box 95500, 1090 HM Amsterdam, The Netherlands.

Objectives: Several investigators have reported decreased expression of glycoprotein Ib on the platelet surface during coronary artery bypass grafting, but others could not confirm this finding. Because platelet glycoprotein Ib functions as an adhesion receptor for von Willebrand factor and other adhesive proteins, this decreased expression may explain excessive postoperative blood loss. In this study the expressions of glycoprotein Ib and other platelet activation markers were studied in the systemic and pericardial blood of seven patients undergoing coronary artery bypass grafting. Pericardial blood was recently shown to have high activation levels of fibrinolytic and coagulation pathways; we hypothesized that this local blood activation might be paralleled by extensive platelet activation and associated disappearance of glycoprotein Ib.
Methods: Expression of platelet surface antigens was determined by whole-blood double-label flow cytometry.
Results: Glycoprotein Ib expression in systemic blood decreased 10% (p = 0.03) from preoperative levels at the start of cardiopulmonary bypass and 30% (p = 0.04) before release of the aortic crossclamp. Expression in pericardial blood at these times decreased by 50% and 51%, respectively (p = 0.003, p = 0.009). No changes were observed in the expression of the platelet activation antigens CD62P (P-selectin, indicating platelet -granular release) and CD63 (indicating lysosomal release) or in binding of monoclonal antibody PAC-1 (detecting the fibrinogen-binding receptor conformation of the glycoprotein IIb-IIIa complex).
Conclusion: Glycoprotein Ib disappeared from the platelet surface during bypass grafting, most notably in pericardial blood. No increased expression of CD62P, CD63, or PAC-1 was found, indicating the absence of general platelet activation.

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