Multispectral imaging of cortical vascular and hemodynamic responses to a shock wave: observation of spreading depolarization and oxygen supply-demand mismatch

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, [Formula: see text]) to the left frontal region in a rat and performed multispectral imaging of the ipsilateral cortex through a cranial window ([Formula: see text]). For the spectral data obtained, we conducted multiple regression analysis aided by Monte Carlo simulation to evaluate vascular diameters, regional hemoglobin concentration ([Formula: see text]), tissue oxygen saturation ([Formula: see text]), oxygen extraction fraction, and light-scattering signals as a signature of cortical spreading depolarization (CSD). Immediately after LISW exposure, [Formula: see text] and [Formula: see text] 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 [Formula: see text]). However, severe hypoxemia was persistently observed during the post-CSD period ([Formula: see text]). 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.