Figure 5.

In vivo sodium fluorescein assay further elucidates changes in BBB permeability with increased barrier permeability following moderate CCI-TBI and rescue of barrier function with anti-ICAM-1/catalase. Sodium fluorescein was administered IV at 48 hrs post-CCI-TBI to evaluate barrier integrity at this time point. The small molecular weight fluorescent tracer was allowed to circulate for 15 min before tissue perfusion and collection. Fluorescent images captured using short wave UV light demonstrate sodium fluorescein leakage into brain tissue in naive ((A), no craniectomy) and sham (B) mice and mice sustaining moderate CCI-TBI events at 48 hr following injury (C) CCI-TBI only, D: CCI-TBI+Anti-ICAM-1/catalase, (E) CCI-TBI+anti-ICAM-1 antibody, and F: CCI-TBI+catalase). The dashed circle in B demarcates where the craniectomy was performed. Sodium fluorescein leakage into the brain extends beyond the area of impact following moderate CCI-TBI, highlighted by white arrowheads. Black arrowheads indicate areas of hemorrhage, edema, or swelling of the brain following injury. Coup and contrecoup mechanisms of injury resulting from CCI-TBI can be appreciated by comparing sodium fluorescein signal detection in the area of impact (top of brain section) to the base of the brain directly opposite of the area of impact in CCI-TBI and CCI-TBI+Catalase groups (C,F).