GpIbα-VWF interactions are required to achieve rapid vessel lumen closure and participate in thrombus resistance to GpIIb/IIIa inhibitors. (A) Representative laser Doppler profiles of mice treated with saline, ATA, or GR during thrombus formation. The black arrow indicates the time of injection of the different inhibitors. (B) Mean CBF at the end of the monitoring period (30 minutes after FeCl₃ application) of mice treated with saline, ATA, or GR during thrombus formation (n = 4 mice/group). (C) Representative immunohistological staining for VWF, CD41 (platelet marker), and 4′6 diamidino-2-phenylindole nuclear staining of MCA of saline-treated mice 20 minutes after FeCl₃-induced MCAo (representative of 10 mice). (D) Representative immunohistological stainings (CD41, VWF, and 4′6 diamidino-2-phenylindole) of MCA from mice that received either saline or ATA during thrombus formation. The yellow dotted line delineates the VWF-rich part of the thrombus. (E) Representative immunohistological images of the MCA 20 minutes after thrombosis in mice that received fluorescently labeled platelets intravenously 10 minutes before FeCl₃ application (representative of 5 mice). In the Xia.B2 group, platelets were incubated with anti-GpIbα Fab (40 µg/mL) before being injected. (F) Quantitative analysis of the proportion of platelets in the VWF-rich part of the thrombus after injection of control or GpIbα-blocked, fluorescently labeled platelets (n = 4 mice/group). (G) Representative laser Doppler profiles of mice treated with saline or ATA during thrombus formation and with GR 20 minutes after MCAo. (H) Mean CBF measured in both groups before and after GR treatment (n = 5 mice/group). ns, not significant.