Abstract
Mild-to-moderate closed-head injury (mmCHI) is an acute disease induced by high-altitudes. It is general practice to transfer patients to lower altitudes for treatment, but the pathophysiological changes at different altitudes following mmCHI remain unknown. The present study simulated acute high-altitude exposure (6,000 m above sea level) in rats to establish a model of mmCHI and recorded their vital signs. The rats were then randomly assigned into different altitude exposure groups (6,000, 4,500 and 3,000 m) and neurological severity score (NSS), body weight (BW), brain magnetic resonance imaging (MRI), brain water content (BWC) and the ratio of BW/BWC at 6, 12 and 24 h following mmCHI, and the glial fibrillary acidic protein levels were analysed in all groups. The results revealed that within the first 24 h following acute high-altitude exposure, mmCHI induced dehydration, brain oedema and neuronal damage. Brain injury in rats was significantly reversed following descent to 4,500 m compared with the results from 6,000 or 3,000 m. The results indicated that subjects should be transported as early as possible. Furthermore, avoiding large-span descent altitude was beneficial to reduce neurological impairment. The examination of brain-specific biomarkers and MRI may further be useful in determining the prognosis of high-altitude mmCHI. These results may provide guidance for rescuing high altitude injuries.