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タイトル砂ネズミ海馬における一過性脳虚血後の遅発性神経細胞壊死に対する低体温の脳保護効果
タイトルヨミスナ ネズミ カイバ ニ オケル イッカセイ ノウキョケツゴ ノ チハツセイ シンケイ サイボウ カイシ ニ タイスル テイタイオン ノ ノウ ホゴ ホウカ
タイトル別表記Amelioration of delayed neuronal death in the gerbil hippocampus by mild hypothermia
作成者山下, 勝弘
作成者ヨミヤマシタ, カツヒロ
作成者別表記Yamashita, Katsuhiro
作成者所属山口大学医学部
内容記述(抄録等)The protective effect of mild hypothemia againt delayed neronal death in sector cornu ammonis 1 (CA1 of the gerbil hippocampus was examined at different body temperatures. Transient forebrain inschmia was induced by occulusion of the bilateral common cartoid arteries for 5 min under halothane anesthsia. The rectal temperature during and 10 min after ischmia was controlled in four separate groups as follows : normothermia group, above 36℃ and below 38℃ ; hypothemia A group, above 35℃ and below 36℃ ; B group, above 34℃ and below 35℃ ; C group, above 33℃ and below 34℃ (n=9 in all groups). Forhistopathological examination of the tissue, the brain was removed from each gerbil at 7 days after transient ischmia, fixed with 10% formaldehyde and embedded in praffin. A coronal section of the dorsal hippocampus was made between 1.4mm and 2.0mm posterior to the bregma and stained with hematoxylin and eosin. The number of non-damaged neurons per 1mm linear length, representative of neuronal density, in sector CA1 was assessed. The mean±SEM neuronal density in 5 non-treated normal gerbils was 254±4/mm. The mean±SEM neuronal density in the normothermia group, hypothrmia above 33℃ and below 35℃ amliorated the exten of ischemic neuronal damage markedly in sector CA1 of the hippocampus. The protective effect of mild hypothemia was also assessed with regard to protein metabolism in neuronal cells. Ubiquition normally exists in all neurons. It removes degenerated proteins produced by ischemia or heat shock and short-lived proteins by binding to them in an ATP-dependent manner. Using affinity-purified monoclonal antibody against ubiquitin, the immunoreactivity in the gerbil hippocampus at 6, 24 and 48 hours after ischmia was examined in normothermia and hypothermia groups. In the normothrmia group, ubiquitin immunoreactivity disappeared in all areas of the hypothermia group, above 33℃ and below 35℃, ubiquitin immunoreactivity in sector CA1 dissappeared at 6 hours, as in the normothermia group. However, it recovered significantly at 24 and 48 hours. It is concluded that the improvement of uniquitin immunoreactivity means improved of short-lived proteins disposal of degenerated proteins after ischemia, which could be one essential part of the mecanism of protection affored by mild hypothermia against delayed neuronal death.
本文言語jpn
主題医学
資料タイプtext
出版者山口大学医学会
出版者ヨミヤマグチ ダイガク イガッカイ
NII資料タイプ学術雑誌論文
査読の有無査読あり
ISSN0513-1731
NCIDAN00243156
学内刊行物(紀要等)山口医学
掲載誌名山口医学
39
6
開始ページ625
終了ページ635
発行日1990-12
著者版/出版社版その他
リポジトリIDB030039000602
地域区分山口大学
URIhttp://www.lib.yamaguchi-u.ac.jp/yunoca/handle/B030039000602