Unfractionated heparin after TBI reduces in vivo cerebrovascular inflammation, brain edema and accelerates cognitive recovery.

Background: Severe traumatic brain injury (TBI) may increase the risk of venous thromboembolic complications; however, early prevention with heparinoids is often withheld for its anticoagulant effect. New evidence suggests low molecular weight heparin reduces cerebral edema and improves neurological recovery following stroke and TBI, through blunting of cerebral leukocyte (LEU) recruitment. It remains unknown if unfractionated heparin (UFH) similarly affects brain inflammation and neurological recovery post TBI. We hypothesized that UFH after TBI reduces cerebral edema by reducing LEU-mediated inflammation and improves neurological recovery. Methods: CD1 male mice underwent either TBI by controlled cortical impact (CCI) or sham craniotomy. UFH (75U/kg or 225U/kg) or vehicle (VEH, 0.9% saline) was administered 2, 11, 20, 27, and 34h after TBI. At 48h, pial intravital microscopy (IVM) through a craniotomy was used to visualize live brain LEUs interacting with endothelium and microvascular FITC-albumin leakage. Neurologic function (Garcia Neurological Test, GNT) and body weight loss ratios were evaluated 24 and 48h after TBI. Cerebral and lung wet-to-dry ratios were evaluated post mortem. ANOVA with Bonferroni correction was used to determine significance (p

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