Optical monitoring of shock wave-induced spreading depolarization and concomitant hypoxemia in rat brain

Okuda, Wataru; Kawauchi, Satoko; Ashida, Hiroshi; Sato, Shunichi; Nishidate, Izumi

doi:10.1117/12.2040899

Cited by 1 publication

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“…In our previous study, we performed transcranial real-time diagnosis of the rat brain exposed to an LISW by using optical fiber-based diffuse reflectance spectroscopy (DRS). 5,14 We observed that, immediately after LISW application, cortical spreading depolarization (CSD) was generated at the site of LISW application and propagated over the entire ipsilateral cortex. This was accompanied by distinct hyperemia/hyperoxemia, but after CSD propagation, long-lasting hypoxemia/oligemia was observed for up to ∼3 h. CSD is a wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water movements, therefore imposing a considerable metabolic workload on the tissue for restoration of imbalanced ions.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2019

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imaging of cortical vascular and hemodynamic responses to a shock wave: observation of spreading depolarization and oxygen supply-demand mismatch," J.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 laserinduced 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 ¼ 4). For the spectral data obtained, we conducted multiple regression analysis aided by Monte Carlo simulation to evaluate vascular diameters, regional hemoglobin concentration (rC Hb ), tissue oxygen saturation (StO 2 ), oxygen extraction fraction, and light-scattering signals as a signature of cortical spreading depolarization (CSD). Immediately after LISW exposure, rC Hb and StO 2 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.

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Section: Introductionmentioning

confidence: 99%