Effects of Isolated and Combined Exposure of the Brain and Lungs to a Laser-Induced Shock Wave(s) on Physiological and Neurological Responses in Rats

Kawauchi, Satoko; Yoshida, Keiichiro; Osawa, Takuya; Muramatsu, Yuriko; Nawashiro, Hiroshi; Karna, Shashi P.; Gupta, Raj K.; Nishidate, Izumi; Sato, Shunichi

doi:10.1089/neu.2022.0101

Cited by 2 publications

(8 citation statements)

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“…The most prominent increase in fluorescence was observed along the pial arteriolar walls in Group 2 (CSD+) rats (Figure 5b) during the period spanning from 10 min to 30 min post‐exposure. This period of intense fluorescence coincided with the early phase of persistent cerebral oligemia/hypoxemia observed in our previous study (Kawauchi et al, 2019, 2022; Sato et al, 2014), suggesting an association of NO production with shock wave‐induced hemodynamic dysfunction in the brain. NOS inhibition (Group 3) caused no significant fluorescence increase at any timepoint analyzed (Figure 6), indicating that the observed NO production was due to NOS activation.…”

Section: Discussionsupporting

confidence: 82%

“…Accordingly, this study consisted of the following four groups: Group 1 (sham control, n = 6), Group 2 (NO imaging with LISW exposure, CSD+, n = 6), Group 3 (NO synthase inhibitor administration and NO imaging with LISW exposure, CSD+, n = 6), and Group 4 (NO imaging with LISW exposure, CSD‐, n = 6). The rats used in this study were all male rats ( n = 30) and no female rats were enrolled to maintain consistency with our previous studies (Jitsu et al, 2021; Kawauchi et al, 2019, 2022; Sato et al, 2014).…”

Section: Methodsmentioning

confidence: 96%

“…The rats used in this study were all male rats (n = 30) and no female rats were enrolled to maintain consistency with our previous studies (Jitsu et al, 2021;Kawauchi et al, 2019Kawauchi et al, , 2022Sato et al, 2014).…”

Section: Animals and Study Designmentioning

confidence: 99%

“…It would be crucial to examine the cause of these hemodynamic abnormalities to fully understand the mechanisms of bTBI. Since LISW is spatially well confined and not accompanied by dynamic pressure (jet), this model allows us to observe the effects of primary blast (the effects of a shock wave itself) locally, in a limited brain region (Jitsu et al, 2021;Kawauchi et al, 2019Kawauchi et al, , 2022Sato et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Our previous study demonstrated the occurrence of cortical spreading depolarization (CSD) in the rat brain exposed to a laser‐induced shock wave (LISW) (Sato et al, 2014). CSD was accompanied by transient (3 ~ 4 min) hyperemia/hyperoxemia, followed by long‐lasting oligemia/hypoxemia in the cortex (Kawauchi et al, 2019, 2022; Sato et al, 2014). It would be crucial to examine the cause of these hemodynamic abnormalities to fully understand the mechanisms of bTBI.…”

Section: Introductionmentioning

confidence: 99%

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In vivo imaging of nitric oxide in the male rat brain exposed to a shock wave

Kawauchi

Inaba

Muramatsu

et al. 2023

J of Neuroscience Research

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While numerous studies have suggested the involvement of cerebrovascular dysfunction in the pathobiology of blast‐induced traumatic brain injury (bTBI), its exact mechanisms and how they affect the outcome of bTBI are not fully understood. Our previous study showed the occurrence of cortical spreading depolarization (CSD) and subsequent long‐lasting oligemia/hypoxemia in the rat brain exposed to a laser‐induced shock wave (LISW). We hypothesized that this hemodynamic abnormality is associated with shock wave‐induced generation of nitric oxide (NO). In this study, to verify this hypothesis, we used an NO‐sensitive fluorescence probe, diaminofluorescein‐2 diacetate (DAF‐2 DA), for real‐time in vivo imaging of male Sprague–Dawley rats' brain exposed to a mild‐impulse LISW. We observed the most intense fluorescence, indicative of NO production, along the pial arteriolar walls during the period of 10–30 min post‐exposure, parallel with CSD occurrence. This post‐exposure period also coincided with the early phase of hemodynamic abnormalities. While the changes in arteriolar wall fluorescence measured in rats receiving pharmacological NO synthase inhibition by nitro‐L‐arginine methyl ester (L‐NAME) 24 h before exposure showed a temporal profile similar to that of changes observed in LISW‐exposed rats with CSD, their intensity level was considerably lower; this suggests partial involvement of NOS in shock wave‐induced NO production. To the best of our knowledge, this is the first real‐time in vivo imaging of NO in rat brain, confirming the involvement of NO in shock‐wave‐induced hemodynamic impairments. Finally, we have outlined the limitations of this study and our future research directions.

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Section: Discussionsupporting

confidence: 82%