Abstract
Introduction. Explosive explosive injuries account for more than 50% of all injuries received in military battles, and the proportion of casualties among the civilian population is also increasing [1]. However, only limited research has been conducted on the pathophysiology of blast-induced brain injury, and the effect of changes in cerebral blood flow (CBF) or cerebral vascular reactivity on blast-induced brain injury has not been investigated [2]. Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after blunt head injury, the effect of secondary injury factors in blast injury is unknown [2]. TBI itself causes cerebral hypoperfusion, reduced oxygen delivery to the brain, excitotoxicity, and disruption of cerebral blood flow autoregulation, which explains the vulnerability of the affected brain to hypoxia and hypotension caused by blood loss [2,3].
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