ADAMTS13 promotes MCA recanalization and reduces ischemic brain injury. A FeCl₃-mediated injury was induced in the MCA of both Adamts13^−/− and Adamts13^+/+ animals to cause a small thrombotic occlusion of the MCA. (A) Absence of ADAMTS13 results in a faster occlusion of the MCA. Time to first occlusion was defined as the time after FeCl₃ application until blood flow dropped below 25%. (B) Averaged postocclusion MCA blood flow profiles reveal that restoration of blood flow was significantly impaired in Adamts13^−/− mice compared with Adamts13^+/+ animals. Administration of rhADAMTS13 5 minutes after occlusion (arrow) restored blood flow. (C) Twenty-four hours after occlusion, cerebral infarctions were determined via TTC staining and planimetric analysis. Infarct sizes were significantly larger in Adamts13^−/− mice than in Adamts13^+/+ mice. Treatment of Adamts13^−/− mice with rhADAMTS13 5 minutes after occlusion significantly reduced infarct sizes. Quantification of the infarct sizes is shown in the left panel, and representative brain sections are shown in the right panel. (n = 10-14 mice/group; *P < .05; **P < .01; compared with Adamts13^−/− mice treated with vehicle.)