Document Detail

Inhaled nitric oxide reduces secondary brain damage after traumatic brain injury in mice.
MedLine Citation:
PMID:  23188422     Owner:  NLM     Status:  MEDLINE    
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.
Nicole A Terpolilli; Seong-Woong Kim; Serge C Thal; Wolfgang M Kuebler; Nikolaus Plesnila
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-11-28
Journal Detail:
Title:  Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism     Volume:  33     ISSN:  1559-7016     ISO Abbreviation:  J. Cereb. Blood Flow Metab.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-01     Completed Date:  2013-03-25     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  8112566     Medline TA:  J Cereb Blood Flow Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  311-8     Citation Subset:  IM    
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MeSH Terms
Blood Pressure / drug effects
Blood-Brain Barrier / injuries,  physiopathology
Brain Edema / drug therapy,  etiology,  physiopathology
Brain Injuries / complications,  drug therapy*,  physiopathology
Brain Ischemia / drug therapy*,  etiology,  physiopathology
Cerebrovascular Circulation / drug effects*
Disease Models, Animal
Endothelium-Dependent Relaxing Factors / pharmacology*
Nitric Oxide / pharmacology*
Reg. No./Substance:
0/Endothelium-Dependent Relaxing Factors; 31C4KY9ESH/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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