Figure 5
Figure 5. Mouse arterial thrombosis models. (A) C57Bl/6 mice of the genotypes indicated at the right of the panel were tested in a carotid artery thrombosis model at FeCl3 concentrations from 2.5% to 15% (10 animals per concentration), as described in “Methods.” Bar heights indicate percent of mice in each group with patent arteries 30 minutes after applying FeCl3. (B) Time to carotid arterial occlusion in wild-type (n = 16), fXI-deficient (n = 12), or fXII-deficient (n = 15) mice in a Rose Bengal-laser injury model, as described in “Methods.” Error bars indicate 1 standard deviation. Time to occlusion is significantly longer for fXI−/− than wild-type mice (*P = .0012), for fXII−/− than wild-type mice (**P = .0001) and for fXII−/− than fXI−/− mice (**P = .0031). (C) Results from the FeCl3 carotid artery thrombosis model (panel A), comparing the effect of treatment with an intravenous infusion of 14E11 (1.0 mg/kg) into wild-type mice () to results for 7.5% and 10% FeCl3 from panel A.

Mouse arterial thrombosis models. (A) C57Bl/6 mice of the genotypes indicated at the right of the panel were tested in a carotid artery thrombosis model at FeCl3 concentrations from 2.5% to 15% (10 animals per concentration), as described in “Methods.” Bar heights indicate percent of mice in each group with patent arteries 30 minutes after applying FeCl3. (B) Time to carotid arterial occlusion in wild-type (n = 16), fXI-deficient (n = 12), or fXII-deficient (n = 15) mice in a Rose Bengal-laser injury model, as described in “Methods.” Error bars indicate 1 standard deviation. Time to occlusion is significantly longer for fXI−/− than wild-type mice (*P = .0012), for fXII−/− than wild-type mice (**P = .0001) and for fXII−/− than fXI−/− mice (**P = .0031). (C) Results from the FeCl3 carotid artery thrombosis model (panel A), comparing the effect of treatment with an intravenous infusion of 14E11 (1.0 mg/kg) into wild-type mice () to results for 7.5% and 10% FeCl3 from panel A.

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