RGS10^−/− mice form larger more stable thrombi. Confocal intravital fluorescence microscopy was performed to follow platelet accumulation (A-B), P-selectin expression (A,C), fibrin deposition (D), and platelet embolization (E) after making small penetrating injuries in cremaster muscle arterioles with a laser in RGS10^−/− mice and littermate controls. Bar graphs represent the CD41⁺ (B) and P-selectin⁺ (C) areas at the end of the 3-minute observation period. N = 78 injuries performed in 11 mice. (D) Fibrin accumulation detected with a fibrin-specific antibody (24 injuries in 3 mice). (E) The mean fluorescence area of platelet clumps passing through a virtual analysis window placed immediately downstream of the injury site. The data were pooled into early (i) and late (ii) time points for analysis. N = 19 injuries for WT and 18 injuries for RGS10^−/− in 3 mice. (Fi) The decline over time in the relative porosity of hemostatic thrombi formed in WT and RGS10^−/− mice infused with caged FITC-albumin. Data are mean ± SEM, 22 injuries in 4 WT mice and 23 injuries in 4 RGS10^−/− mice. (Fii) ∆MFI measured 180 seconds after injury. ∆MFI, increment in mean fluorescence intensity measured over the entire thrombus at 15-second intervals immediately after a light flash that causes the albumin to fluoresce.