| Project/Area Number | 05671268 |
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Ehime University |
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Principal Investigator |
ARARI Tatsuru Ehime University, School of Medicine, Professor, 医学部, 教授 (50033436)
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| Co-Investigator(Kenkyū-buntansha) |
DOTE Kentaro Ehime University, School of Medicine, Assistant Professor, 医学部・附属病院, 講師 (00172239)
AMAKAWA Kazuhiko Ehime University, School of Medicine, Assistant Instructor, 医学部・附属病院, 助手 (50136313)
足立 尚澄 (足立 尚登) 愛媛大学, 医学部・附属病院, 助手 (50253315)
井上 裕昭 愛媛大学, 医学部, 助手 (60263927)
藤谷 太郎 愛媛大学, 医学部・附属病院, 助手 (20229016)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed(Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost : ¥2,200,000)
Fiscal Year 1995 : ¥300,000 (Direct Cost : ¥300,000)
Fiscal Year 1994 : ¥300,000 (Direct Cost : ¥300,000)
Fiscal Year 1993 : ¥1,600,000 (Direct Cost : ¥1,600,000)
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| Keywords | Cerebral ischemia / Lidocaine / Amino acids / Hippocampus / Microdialysis / Mongolian gerbils / Direct current potential / Anoxic depolarization / 海馬CA1領域 / グルタミン酸 / 脳室内投与 / ナトリウムチャンネル遮断薬 / プロカインアミド / ダントロレン |
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| Research Abstract |
Extracellular levels of amino acids in the hippocampal CA1 region of the gerbil were analyzed by a microdialysis-HPLC procedure. Transient forebrain ischemia produced significant increase in aspartate, glutamate, glycine and taurine (760%, 1070%, 190% and 1210%, respectively), and neuronal blockade by perfusion with a lidocaine (4 mmol/L) -containing medium resulted in 67%, 79%, 58% and 59% reduction in the peak values of each amino acid, respectively. Centrally administered lidocaine (4.0 mu mol) produced a 140% prolongation of its onset latency of anoxic depolarization. On the other hand, an intracerebroventricular administration of lidocaine, 0.8 mu mol or more, produced a protective effect against delayd damage of hippocampal CA1 pyramidal cells, which was caused by bilateral carotid artery occlusion for 4 min. The results suggest that lidocaine may protect neurons against ischemic damage, by preventing the ischemia-induced rise of extracellular concentration of excitatory amino acid.
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