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Abstract
Heparin may induce platelet activation and even heparin-induced thrombocytopenia. Lepirudin has been approved for HIT treatment. We speculated that lepirudin inhibits platelet function under high shear and the platelet thrombin receptor PAR-1 better than heparin. Thrombin-inducible platelet adherence under high shear conditions and the expression of PAR-1 were studied after samples from healthy donors were exposed in vitro to increasing concentrations of unfractionated heparin or lepirudin. Compared to baseline and to lepirudin, heparin induced platelet P-selectin expression (p = 0.04). Platelet adherence increased slightly in the presence of lepirudin, but not heparin (p = 0.04). Thrombin-inducible platelet aggregate formation and consecutive adherence under high shear conditions was inhibited by both anticoagulants (p = 0.004). Further, heparin and lepirudin inhibited thrombin-inducible cleavage and internalization of PAR-1 at a dosage of 1.0 U/ml and 1.6 µg/ml, respectively (p = 0.004). Thus, heparin and lepirudin inhibit thrombin-inducible platelet activation in vitro to a similar extent.