Figure 7
Figure 7. Defective thrombus formation in vitro and in vivo. (A) Whole blood from busulfan-treated wt mice (+/+) or MYH9Δ mice (−/−) was anticoagulated with hirudin (100 U/mL) and perfused through collagen-coated glass capillaries at a shear rate of 3000 s−1. Scanning electron microscopy imaging was performed after 2-minute perfusion and images are representative of 3 experiments. Bars, 20 μm (top panels) and 5 μm (bottom panels). (B) FeCl3-induced injury was performed in the carotid of busulfan-treated wt mice (+/+) or MYH9Δ mice (−/−) and the thrombus growth was video recorded. Images are representative of 8 mice, at time 600 seconds following injury (original magnification × 45). (C) Time courses of the embolus surface area measured by the fluorescence passing through the region of interest (white square in the insert), downstream of the thrombus. Busulfan-treated wt mice (gray curve) and MYH9Δ mice (black curve); n = 8, P < .001 (Student paired t test).

Defective thrombus formation in vitro and in vivo. (A) Whole blood from busulfan-treated wt mice (+/+) or MYH9Δ mice (−/−) was anticoagulated with hirudin (100 U/mL) and perfused through collagen-coated glass capillaries at a shear rate of 3000 s−1. Scanning electron microscopy imaging was performed after 2-minute perfusion and images are representative of 3 experiments. Bars, 20 μm (top panels) and 5 μm (bottom panels). (B) FeCl3-induced injury was performed in the carotid of busulfan-treated wt mice (+/+) or MYH9Δ mice (−/−) and the thrombus growth was video recorded. Images are representative of 8 mice, at time 600 seconds following injury (original magnification × 45). (C) Time courses of the embolus surface area measured by the fluorescence passing through the region of interest (white square in the insert), downstream of the thrombus. Busulfan-treated wt mice (gray curve) and MYH9Δ mice (black curve); n = 8, P < .001 (Student paired t test).

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