FcγRIIa amplifies thrombus formation. Laminar flow chambers were coated with 50 µg/mL type I fibrillar collagen and blocked with Hank balancing salt solution containing 0.1% BSA. Whole blood from WT (FcγRIIa^neg) and transgenic (FcγRIIa^pos) mice was anticoagulated with heparin and PPACK, labeled with mepacrine, and perfused under conditions of either arterial (2888 s⁻¹) or venous (444 s⁻¹) shear. Images of platelet adhesion and accumulation were acquired using epifluorescence microscopy in real time at a rate of 1 frame per second. (A,C) Representative time-course images of platelet adhesion and accumulation on collagen at a shear rate of 2888 s⁻¹ (A) or 444 s⁻¹ (C). (B,D) Quantification of platelet thrombi formed at 2888 s⁻¹ (B) or 444 s⁻¹ (D) was performed using Metamorph software. Results are expressed as the mean percentage of surface coverage (left panels) or total integrated fluorescence intensity (right panels) ± SEM (n ≥ 7 per group). Statistically significant differences between the means were determined using the Student t test. Note that thrombus formation was significantly increased (*P < .05) for FcγRIIa^pos platelets compared with their WT murine counterparts under conditions of both arterial and venous flow.