Continuous infusion of XXXX postinjury significantly ameliorates @entity16 following traumatic brain injury.

@entity131 @entity870 @entity39 @entity16 @entity51 @entity205 @entity460 @entity35
@entity131 ( @entity131 ) results in the rapid @entity39 of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the original damage resulting in significant @entity51 . Recent reports from our lab demonstrate that a bolus injection of the immunosuppressant @entity205 ( @entity870 ) is neuroprotective following @entity131 . @entity870 transiently inhibits the opening of the mitochondrial permeability transition pore and maintains @entity460 homeostasis in isolated mitochondria. The present study utilized a unilateral controlled cortical impact model of @entity131 to assess whether the neuroprotective effects of @entity870 could be extended by chronic infusion. Adult @entity35 were subjected to a moderate (2 mm) cortical deformation and the extent of @entity16 was assessed using modern stereological techniques. Animals were administrated a 20 mg/kg intraperitoneal bolus of @entity870 or vehicle 15 min postinjury and osmotic minipumps were implanted subcutaneously to deliver @entity870 (4.5 or 10 mg/kg/day) or vehicle. All animals receiving @entity870 demonstrated a significant reduction in lesion volume, with the highest dose offering the most neuroprotection (74% reduction in lesion volume). These results extend our previous findings and demonstrate that chronic infusion of @entity870 is neuroprotective following @entity131 . These findings also suggest that the mechanisms responsible for tissue @entity39 following @entity131 are amenable to manipulation.
