作者: Usmah Kawoos , Richard M. McCarron , Mikulas Chavko
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摘要: Blast-induced traumatic brain injury (bTBI) is associated with acute and possibly chronic elevation of intracranial pressure (ICP). The outcome after TBI dependent on the progression complex processes which are mediated by oxidative stress. So far no effective pharmacological protection against exists. In this study, rats were exposed to a single or repetitive blast overpressure (BOP) at moderate intensities 72 110 kPa in compressed air-driven shock tube. degree duration increase ICP was proportional intensity frequency exposure(s). most cases, dose antioxidant N-acetylcysteine amide, NACA (500 mg/kg) administered intravenously 2 h exposure BOP significantly attenuated blast-induced ICP. A not improving group animals that subjected exposures same day. group, two treatments 4 post-BOP resulted significant attenuation elevated Treatment prior completely prevented findings indicate stress plays an important role as treatment ameliorated increase, frequently related poor functional recovery TBI.