Recent data have implicated the importance of nitric oxide (NO) in the pathophysiology of traumatic brain injury (TEl) [2, 3, 4, 5]. After controlled cortical impact injury, levels of neuronal nitric oxide synthase (nNOS), mRNA, and protein increased by 2h after trauma . Using a moderate F-P model, Wada and colleagues  reported the immediate but transient increase in constitutive nitric oxide synthase (cNOS) activity within the histopathologically injured cortical region.This increase in cNOS activity was followed by a sustained reduction in cNOS activity below control levels. Inducible NOS (iNOS) activity was also reported to increase at 7 days after TEl 
KeywordsNitric Oxide Traumatic Brain Injury Therapeutic Hypothermia cNOS Activity Matic Brain Injury
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