The effects of aprotinin on platelets in vitro using whole blood flow cytometry

We sought to evaluate the effects of aprotinin on the number and function o f the platelet glycoprotein (GP) IIb-IIIa receptor and on the expression of P-selectin in vitro in order to gain insight into the potential mechanisms involved in the platelet-protective action of aprotinin during cardiopulmo nary bypass. Aprotinin at 50 to 200 kallikrein inhibiting units/mL decrease d the expression of activated GP IIb-IIIa complex in response to adenosine diphosphate or thrombin receptor activator peptide 6 in a dose-dependent ma nner in both citrated and heparinized whole blood experiments. Aprotinin in hibited adenosine diphosphate-induced platelet aggregation, but it exhibite d no effect on the expression of GP IIIa and P-selectin. These results indi cate that aprotinin interferes with the platelet fibrinogen receptor functi on during pharmacological activation. Reduced aggregability and platelet ad hesion to fibrinogen adsorbed to synthetic surfaces in the presence of apro tinin may prevent platelet consumption during clinical cardiopulmonary bypa ss. This in vitro study demonstrates that aprotinin decreases the agonist-i nduced expression of activated GP IIb-IIIa receptors that play a major role in platelet aggregation and adhesion to biomaterial surfaces. Implications : This in vitro study demonstrates that aprotinin decreases the agonist-ind uced expression of activated glycoprotein IIb-IIIa receptors that play a ma jor role in platelet aggregation and adhesion to biomaterial surfaces.