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1525638 
Journal Article 
Inhaled nitric oxide reduces secondary brain damage after traumatic brain injury in mice 
Terpolilli, NA; Kim, SW; Thal, SC; Kuebler, WM; Plesnila, N 
2013 
Yes 
Journal of Cerebral Blood Flow and Metabolism
ISSN: 0271-678X
EISSN: 1559-7016 
33 
2 
311-318 
English 
23188422 
WOS:000314739600020 
Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood-brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients. 
brain edema; brain trauma; cerebral blood flow; microcirculation; nitric oxide