Pathophysiology and Treatment of Brain Ischemia
| Project/Area Number |
62440063
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Yamaguchi University |
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Principal Investigator |
TAKESHITA Hiroshi School of Medicine . Professor, 医学部, 教授 (50034898)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Ikuo School of Medicine . Assistant, 医学部, 助手 (30145536)
NAKAKIMURA Kazuhiko Yamaguchi University Hospital . Assistant, 医学部附属病院, 助手 (50180261)
ISHIKAWA Toshizoh School of Medicine . Assistant, 医学部, 助手 (90034991)
SAKABE Takefumi School of Medicine . Associated, 医学部, 助教授 (40035225)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥10,000,000 (Direct Cost: ¥10,000,000)
Fiscal Year 1988: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥8,000,000 (Direct Cost: ¥8,000,000)
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| Keywords | Brain Ischemia / Local Cerebral Blood Flow / Local Cerebral Glucose Utilization / Ca Accumulation / Receptor Binding / 記憶障害 |
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| Research Abstract |
The purpose of this study is to explore pathophysiological basis of cerebral ischemia with different methods and approaches, and to examine therapeutic interventions including calcium entry blocker. First, the effects of halothane and isoflurane on the post-ischemic hypoperfusion and hypometabolism in global ischemia for 15min were examined in rats, and it was found that the anesthetics with cerebral metabolic depressing action might reduce post-ischemic circulatory and metabolic derangement. Second, selective neuronal necrosis and accumulation of ^<45>Ca (autoradiography) were examined in rats rendered to global ischemia for 10min and it was found that neuronal death of CA_1 and CA_4 area of hippocampus occured 7 days after ischemia, being accompanied by accumulation of calcium. Third, the post-ischemic changes in behavior and memory in relation to hippocampal damage and receptor binding of neurotransmitters (acethylcholine and glutamate) were evaluated in rats rendered to cerebral ischemia for 10min. Memory disturbance was reduced by pentobarbital and nimodipine. Accumulation of calcium in the discrete brain regions was also measured by the atomic absorption flame photometry, and it was found that accumulation of calcium in the hippocampus was observed on the 3rd days after cerebral ischemia, but the values did not reach statistical significance. Receptor binding of acethylcholine (^3H-QNB) and glutamate (^3H-L-Glutamate), which are closely related to memory function, were remained unchaged in the cerebral cortex and hippocampus by nimodipine, while rats showed significant reduction of receptor binding. These results indicate that pentobarbital and nimodipine improved post-ischemic disturbances of memory function which can be related to receptor function of acethylcholine and/or glutamate.
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Report
(3 results)
Research Products
(13 results)
