Overpressure blast-wave induced brain injury elevates oxidative stress in the hypothalamus and catecholamine biosynthesis in the rat adrenal medulla

•A single OBI was performed in rats to assess the activation of hypothalamic sympatho-adrenal-medullary axis.•Adrenal medullary catecholamine synthetic enzymes and NPY protein expression as well as plasma NE were elevated.•NADPH oxidase activity was increased in the hypothalamus.•TH protein was elevated in the NTS. Explosive overpressure brain injury (OBI) impacts the lives of both military and civilian population. We hypothesize that a single exposure to OBI results in increased hypothalamic expression of oxidative stress and activation of the sympatho-adrenal medullary axis. Since a key component of blast-induced organ injury is the primary overpressure wave, we assessed selective biochemical markers of autonomic function and oxidative stress in male Sprague Dawley rats subjected to head-directed overpressure insult. Rats were subjected to single head-directed OBI with a 358kPa peak overpressure at the target. Control rats were exposed to just noise signal being placed at ~2m distance from the shock tube nozzle. Sympathetic nervous system activation of the adrenal medullae (AM) was evaluated at 6h following blast injury by assessing the expression of catecholamine biosynthesizing enzymes, tyrosine hydroxylase (TH), dopamine-β hydroxylase (DβH), neuropeptide Y (NPY) along with plasma norepinephrine (NE). TH, DβH and NPY expression increased 20%, 25%, and 91% respectively, following OBI (P