Background and objective: Bleeding is one of the major complications of cardiopulmonary bypass (CBP) during cardiac surgery. A platelet function defect seems to be the main cause of the hemostatic problems associated with CBP. Controversial results have been reported concerning the possible protective mechanism of action of aprotinin on platelets.
Design and methods: In this study we investigated the effect of two different dosages of aprotinin (high and pump-prime-only dose) on platelet reactivity in vitro and adhesion, activation and aggregation receptors on the platelet surface.
Results: The results obtained from 53 patients undergoing CBP showed a significantly deficient platelet aggregation in response to agonist in all groups without differences between aprotinin treated or not treated patients. No changes in platelet surface expression of glycoprotein (GP) IIb-IIIa, GPIb, GPIV and P-selectin, were observed during CBP between patients treated with aprotinin or not.
Interpretation and conclusions: These data suggest that inadequate platelet function induced by CBP is not a defect intrinsic to the platelet. We conclude that the hemostatic effect of aprotinin, regardless of the dose employed, is not mediated by protection of platelet function.