Effect of FcRγ deficiency on platelet tethering, stable adhesion, and thrombus formation on a collagen substrate. DiOC6-loaded (1 μM) whole blood collected into hirudin (100 μg/mL) (A) or into CTI (40 μg/mL) (C) from wild-type or FcRγ–/– mice was perfused through collagen-coated (2.5 mg/mL) microcapillary tubes for 3 minutes at 500 s–1. The images are representative of single platelets or thrombi formed after 3 minutes of blood perfusion. (B) The number of platelets (mean ± SEM) tethering to the matrix and subsequently forming stationary adhesion contacts was quantitated as described in “Materials and methods.” (D) Following blood perfusion over the collagen matrix, the thrombi were fixed with 4% paraformaldehyde, then imaged by confocal microscopy (3 to 6 fields per microslide, n = 3 for each condition). The total volume of thrombi formed per field (mean ± SEM) was determined as described in “Materials and methods.” Thrombi formed from FcRγ–/– mice were reduced in size (*P < .025; n = 3) compared with thrombi formed from wild-type controls.
