Abstract
Blast-induced traumatic brain injury has been a recent major concern in neurotraumatology. However, its pathophysiology and mechanism are not understood partly due to insufficient information on the brain pathophysiology during/immediately after shock wave exposure. We transcranially applied a laser-induced shock wave (LISW, ∼19 Pa · s) to the left frontal region in a rat and performed multispectral imaging of the ipsilateral cortex through a cranial window (n = 4). For the spectral data obtained, we conducted multiple regression analysis aided by Monte Carlo simulation to evaluate vascular diameters, regional hemoglobin concentration (rCHb), tissue oxygen saturation (StO2), oxygen extraction fraction, and light-scattering signals as a signature of cortical spreading depolarization (CSD). Immediately after LISW exposure, rCHb and StO2 were significantly decreased with distinct venular constriction. CSD was then generated and was accompanied by distinct hyperemia/hyperoxemia. This was followed by oligemia with arteriolar constriction, but it soon recovered (within ∼20 min). However, severe hypoxemia was persistently observed during the post-CSD period (∼1 h). These observations indicate that inadequate oxygen supply and/or excessive oxygen consumption continued even after blood supply was restored in the cortex. Such a hypoxemic state and/or a hypermetabolic state might be associated with brain damage caused by a shock wave.