An Additional Mechanism of Action of Abciximab: Dispersal of Newly Formed Platelet Aggregates

Background: The ability of abciximab to prevent fibrinogen binding to activated platelets indicates it may also promote dissolution of platelet-rich thrombi. The present study examined the capacity of abci-ximab to reverse platelet aggregation in vitro. Methods and Results: Experiments were performed on blood from healthy non-medicated donors. Platelet aggregate formation and disaggregation were monito-red turbidimetrically. Platelet-bound fibrinogen was measured by flow cytometry. For disaggregation studies, platelets were first stimulated with either ADP or the 11-mer thrombin receptor activating peptide (TRAP), then varying amounts of abciximab were added at periodic intervals after agonist addition. Platelet disaggregation was detected by comparing the extent of light transmittance at 4 min after addition of either abciximab or saline to PRP. ATP release was simultaneously monitored by chemi-luminescence. When added 1 min after low concentrations of ADP, abciximab rapidly (