FXII deficiency reduces infarct volume and edema after tPA treatment in thrombotic stroke without increasing the risk of intracerebral hemorrhage. (A) Representative images of coronal sections of show cerebral hemorrhage 24 hours after stroke in mice treated with vehicle or tPA in WT and FXII^−/− mice. At 2 hours after stroke onset, mice received tPA (10 mg/kg) or saline vehicle. (B) Volumes of intracerebral hemorrhage were quantified with hemoglobin assay at 24 hours after stroke. Data are presented as mean ± SEM, n = 8. **P < .01; ***P < .001. (C) Quantitative analysis of brain edema at 24 hours after ischemic stroke. Data are presented as mean ± SEM, n = 8. *P < .05. (D) Representative coronal sections of 2,3,5-triphenyltetrazolium chloride–stained brain sections of mice at 24 hours after ischemic stroke treated with vehicle or tPA in WT and FXII^−/− mice. (E) Quantitative analysis of infarct volume at 24 hours after ischemic stroke. Data are presented as mean ± SEM, n = 8. *P < .05. (F) Effects of FXII inhibition on tPA-induced neurological dysfunction after ischemic stroke. Neurological severity score was evaluated 24 hours after stroke in WT and FXII^−/− mice treated with saline or tPA (10 mg/kg). Data are presented as mean ± SEM, n = 5-8. *P < .05.