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.
Due to considerable increase in the terrorism using explosive devices, blast-induced traumatic brain injury (bTBI) receives much attention worldwide. However, little is known about the pathology and mechanism of bTBI. In our previous study, we found that cortical spreading depolarization (CSD) occurred in the hemisphere exposed to a laser- induced shock wave (LISW), which was followed by long-lasting hypoxemia-oligemia. However, there is no information on the events occurred in the contralateral hemisphere. In this study, we performed multichannel fiber-based diffuse reflectance spectroscopy for the rat brain exposed to an LISW and compared the results for the ipsilateral and contralateral hemispheres. A pair of optical fibers was put on the both exposed right and left parietal bone; white light was delivered to the brain through source fibers and diffuse reflectance signals were collected with detection fibers for both hemispheres. An LISW was applied to the left (ipsilateral) hemisphere. By analyzing reflectance signals, we evaluated occurrence of CSD, blood volume and oxygen saturation for both hemispheres. In the ipsilateral hemispheres, we observed the occurrence of CSD and long-lasting hypoxemia-oligemia in all rats examined (n=8), as observed in our previous study. In the contralateral hemisphere, on the other hand, no occurrence of CSD was observed, but we observed oligemia in 7 of 8 rats and hypoxemia in 1 of 8 rats, suggesting a mechanism to cause hypoxemia or oligemia or both that is (are) not directly associated with CSD in the contralateral hemisphere.
Blast-induced traumatic brain injury is a growing concern, but its underlying pathophysiology and mechanism are still
unknown. Thus, study using an animal model is needed. We have been proposing the use of a laser-induced shock wave
(LISW), whose energy is highly controllable and reproducible, to mimic blast-related injury. We previously observed the
occurrence of spreading depolarization (SD) and prolonged hypoxemia in the rat brain exposed to an LISW. However,
the relationship between these two events is unclear. In this study, we investigated the spatiotemporal characteristics of
hypoxemia and SD to examine their correlation, for which multichannel fiber measurement and multispectral imaging of
the diffuse reflectance were performed for the rat brain exposed to an LISW. We also quantified tissue oxygen saturation
(StO2) in the hypoxemic phase, which is associated with possible neuronal cell death, based on an inverse Monte Carlo
simulation. Fiber measurement showed that the region of hypoxemia was expanding from the site of LISW application to
the distant region over the brain; the speed of expansion was similar to that of the propagation speed of SD. Simulation
showed that oxygen saturation was decreased by ~40%. Multispectral imaging showed that after LISW application, a
vasodilatation occurred for ~1 min, which was followed by a long-lasting vasoconstriction. In the phase of
vasoconstriction, StO2 declined all over the field of view. These results indicate a strong correlation between SD and
hypoxemia; the estimated StO2 seems to be low enough to induce neuronal cell death.
Access to the requested content is limited to institutions that have purchased or subscribe to SPIE eBooks.
You are receiving this notice because your organization may not have SPIE eBooks access.*
*Shibboleth/Open Athens users─please
sign in
to access your institution's subscriptions.
To obtain this item, you may purchase the complete book in print or electronic format on
SPIE.org.
INSTITUTIONAL Select your institution to access the SPIE Digital Library.
PERSONAL Sign in with your SPIE account to access your personal subscriptions or to use specific features such as save to my library, sign up for alerts, save searches, etc.