1991 Fiscal Year Final Research Report Summary
Induction and Identification of Endogenous Anti-Ischemic Mechanisms (Factors)
| Project/Area Number |
63440058
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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 | Nigata University |
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Principal Investigator |
SHIMOJI Koki Niigata University School of Medicine, Professor, 医学部, 教授 (30040158)
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| Co-Investigator(Kenkyū-buntansha) |
DENDA Sadahei Niigata University School of Medicine, Assistant, 医学部, 助手 (20197833)
TAGA Kiichiro Niigata University Hospital, Assistant, 医学部附属病院, 助手 (00163329)
FUJIWARA Naoshi Niigata University Hospital, lecturer, 医学部附属病院, 講師 (70181419)
ENDOH Hiroshi Niigata University Hospital, Lecturer, 医学部附属病院, 講師 (90168831)
FUKUDA Satoru Niigata University School of Medicine, Assistant Professor, 医学部, 助教授 (30116751)
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| Project Period (FY) |
1988 – 1991
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| Keywords | Brain Injury / Anti-Ischemic Activity / Intracellular Free Calcium / Nerve Growth Factor / Regional Metabolic Activity |
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| Research Abstract |
We have previously suggested that artificial minor brain injury induces certain endogenous anti-ischemic mechanisms in the mouse brain. In this study, we examined the survival rate of mice following brain ischemia and characterized the endogenous anti-ischemic activities induced by minor brain injury. The survival rates following incomplete brain ischemia was improved during 1 to 2 weeks following artificial brain injury in the mice. Artificial brain injury also improved the survival from the lidocain-induced seizure. Post-ischemic increase in regional metabolic activity was attenuated in the injured mouse brain. The direct injection of nerve growth factor (NGF), one of neurotropic factors, into the brain tissue did not improve the survival rate of the mice following brain ischemia. On the other hand, we found that Ca^<2+> overload in cytosol may relate to irreversible dysfunction of neurons in hippocampal slices exposed to hypoxia and the increase in intracellular free Ca^<2+> concentration induced by hypoxia in the absence of glucose was attenuated in the vicinity of lesion site in hippocampal CA1 region of mouse brain slices. The results suggest that the anti-ischemic mechanisms may be activated during 1 to 2 weeks in the recovering process from brain injury and may be protective against lidocaine-induced seizure and hypermetabolism following brain ischemia. The origin of anti-ischemic activity may be not assigned to NGF, but certain factor (s) may be produced in the lesion site to attenuate the increase in intracellular free Ca^<2+> concentration, protecting the ischemic cell damage.
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