title: Inhaled nitric oxide reduces secondary brain damage after traumatic brain injury in mice.
abstract: 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.
authors.affiliation: Department of Neurosurgery, University of Munich Medical Center, Munich, Germany.
authors.forename: Nicole A
authors.initials: NA
authors.lastname: Terpolilli
authors.forename: Seong-Woong
authors.initials: SW
authors.lastname: Kim
authors.forename: Serge C
authors.initials: SC
authors.lastname: Thal
authors.forename: Wolfgang M
authors.initials: WM
authors.lastname: Kuebler
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Plesnila
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001812:Blood-Brain Barrier / Q000293:injuries / Q000503:physiopathology; D001929:Brain Edema / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004195:Disease Models, Animal; D045462:Endothelium-Dependent Relaxing Factors / Q000494:pharmacology*; D006801:Humans; D008297:Male; D051379:Mice; D009569:Nitric Oxide / Q000494:pharmacology*
chemical_list: D045462:Endothelium-Dependent Relaxing Factors; D009569:Nitric Oxide