1995 Fiscal Year Final Research Report Summary
Effects of centrally administered agents on ischemia induced brain damage
| 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)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Cerebral ischemia / Lidocaine / Amino acids / Hippocampus / Microdialysis / Mongolian gerbils / Direct current potential / Anoxic depolarization |
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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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