Hypothermia during Ischemia Protects against Neuronal Death but Not Acute Brain Edema following Transient Forebrain Ischemia in Mice

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  • Doshi Masaru
    Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Teikyo University
  • Kuwatori Yudai
    Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Teikyo University
  • Ishii Yoko
    Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences for Research, University of Toyama
  • Sasahara Masakiyo
    Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences for Research, University of Toyama
  • Hirashima Yutaka
    Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Teikyo University

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C57BL/6J mice are widely used as a background strain for genetic alterations and have been valuable for investigating the molecular mechanism of selective neuronal death following transient forebrain ischemia, which was induced by occlusion of bilateral common carotid arteries (BCCA). Hypothermia (HT) during ischemia has been shown to protect against neuronal death in several experimental models of cerebral ischemia including that induced by BCCA occlusion in C57BL/6J mice. In this study, we demonstrated that brain edema, one of the most important disorders following cerebral ischemia, occurred in the forebrain before neuronal death in the hippocampus and was not prevented by HT during cerebral ischemia induced by BCCA occlusion in C57BL/6J mice. Our results indicate that neuronal death and acute brain edema were induced by different mechanisms in the BCCA occlusion and reperfusion C57BL/6J mouse model, suggesting that our model with and without HT during cerebral ischemia may be a useful tool for the investigation of the specific mechanism of brain edema and neuronal death, respectively.

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