The nature of the supposed effects of cardiopulmonary bypass (CPB) on defects in platelet function remains controversial, however, cardiac surgery is believed to be associated with a disruption of the haemostatic system. We employed whole blood flow cytometry to evaluate the possible alterations in the expression of platelet surface membrane glycoproteins in resting and thrombin- or ADP-activated platelets in peripheral blood. As monitored by the use of monoclonal antibodies directed against glycoproteins GPIb, GPIIIa, GPIIbIIIa complexes and P-selectin, circulating blood platelets subjected to extracorporeal circulation were characterized by: a/ time-dependent increase in platelet surface P-selectin, b/ paralleled marked reductions in GPIb and GPIIIa, c/ increased microparticle fraction with no platelet clumping. In comparison to circulating blood platelets collected during CPB, the alterations in platelet P-selectin in post-surgery blood (20 h after bypass) were negligible. We observed the loss in platelet reactivity at every time point of CPB, both in response to time-driven spontaneous anticoagulant-induced activation and following the in vitro action of thrombin and ADP; these depressions occurred with respect to all the monitored platelet surface antigens and remained least marked in post-surgery blood.Our results seem to furnish support for a novel outlook on the molecular mechanisms of the altered expression of platelet surface membrane receptors during CPB. We suggest that (1) markedly deficient platelet reactivity in response to agonist-induced platelet activation, (2) loss of platelet surface membrane glycoproteins GPIb and GPIIIa, (3) enhanced expression of surface membrane P-selectin, and (4) increased number of platelet microparticles point to platelet increased consumption/rupture, degranulation, membrane protein shedding, or all of the above effects as major contributors to altered expression of platelet membrane receptors in CPB patients. Noteworthy, a markedly depressed number/expression of platelet fibrinogen receptor, which, in turn, became augmented in post-surgery blood, implies that CPB can make peripheral blood platelets more vulnerable to pro-aggregatory action of agonists in vivo. This last observation seems critical since it validates the suspicion of the enhanced risk for early occlusion of vein bypass grafts in patients undergoing coronary artery surgery.

Keywords: Cardiopulmonary Bypass, Coronary Artery Disease, platelet receptors, Platelet Activation, platelet consumption/rupture, release reaction, adhesion receptors