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The Effect of Hydrogen Gas on a Mouse Bilateral Common Carotid Artery Occlusion

Part of the Acta Neurochirurgica Supplement book series (NEUROCHIRURGICA,volume 118)

Abstract

In recent studies, molecular hydrogen selectively reduced the levels of hydroxyl radicals in vitro and exerted a therapeutic anti-oxidant activity in a rat middle cerebral artery occlusion model. The aim of this study was to investigate the effect of hydrogen gas on a mouse bilateral common carotid artery occlusion (BCCAO) model. Male C57BL/6J mice were subjected to transient BCCAO with a nontraumatic aneurysm clip. The mice were divided into three groups: sham, BCCAO, and BCCAO treated with 1.3 % hydrogen gas. Cerebral blood flow (CBF) in the cortex was measured sequentially for both hemispheres with a non-­invasive and noncontact laser Doppler blood perfusion imager during the procedure. Vital signs were also recorded. Oxidative stress evaluated by measuring the level of 8-hydroxy-2’-deoxyguanosine (8-OHdG), neuronal injury in the hippocampal CA1 sector, and brain water content were assessed 24 h after ischemia. The hydrogen gas treatment had no significant effect on vital signs or CBF values. However, the reduction of the expression of 8-OHdG, the decrease in the neuronal injury in the hippocampal CA1 sector, and the attenuation in brain water content were observed in hydrogen-treated mice. In conclusion, hydrogen gas might be effective in a mouse BCCAO model.

Keywords

  • Hydrogen
  • Bilateral common carotid artery occlusion
  • Mouse
  • Ischemia/reperfusion injury
  • Brain edema

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Acknowledgments

This study was supported by a research grant from The General Insurance Association of Japan.

Conflict of InterestWe declare that we have no conflict of interest.

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Correspondence to Kimihiro Nagatani .

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© 2013 Springer-Verlag Wien

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Nagatani, K. et al. (2013). The Effect of Hydrogen Gas on a Mouse Bilateral Common Carotid Artery Occlusion. In: Katayama, Y., Maeda, T., Kuroiwa, T. (eds) Brain Edema XV. Acta Neurochirurgica Supplement, vol 118. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1434-6_10

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  • DOI: https://doi.org/10.1007/978-3-7091-1434-6_10

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  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-7091-1433-9

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