Study on pathophysiology of cerebral hypoxia by means of the brain slice technique and the regional perfusion technique
| Project/Area Number |
60480345
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Niigata 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) |
HOKARI Tamaki Niigata University School of Medicine, Assistant, 医学部付属病院, 助手 (10173577)
HASHIBA Masao Niigata University School of Medicine, Lecturer, 医学部付属病院, 講師 (30108047)
ENDOH Hiroshi Niigata University school of Medicine, Assistant, 医学部, 助手 (90168831)
丸山 洋一 新潟大学, 医学部付属病院, 講師 (00111724)
HIGASHI Hideho Kurume University School of Medicine, Associate professor, 医学部, 助教授 (10098907)
MARUYAMA Yoichi Niigata University School of Medicine, Lecturer
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1987: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1986: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1985: ¥3,600,000 (Direct Cost: ¥3,600,000)
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| Keywords | Brain slice / Hippocampus / Hypoxia / Membrane potential / Brain injury / Anti-ischemic activity / 麻酔薬 / 海馬CA1ニューロン / 脳局所灌流 |
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| Research Abstract |
Study I: The activities of the hippocampal CAl neurons in rat brain slices were investigated by intracellular recording under hypoxic and high potassium conditions of superfuson media. By superfusion of the hypoxic (95%N_2-5%CO_2 equilibrated) medium, a small hyperpolarization, a slow and gradual depolarization and a rapid depolarization were spquentially oserved in a majority of the neurons. The initial hyperpolarization induced by hypoxia was not blocked by superfusion with voltage-dependent K-^+-channel blockers (4-aminopyridine, tetraethylammonium, barium, cesium) and by intracellural injection of EGTA. Therefore, The hypoxia-induced hyperpolarization may be brought about by the increase in voltage-independent K^+ conductivities, e.g., ATP-sensitive and/or Na-activated K^+ conductivities. The slow and gradual depolarization and the rapid depolarization were mimicked by superfusion with high pottasium media. In the presence of Ca^<2+> blockers, the membrane activities partially rema
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ined even after 1.5min of 60mM K^+ loading. These facts suggest that the extracellulae K^+ level increases slowly to cause slow membrane depolarization with hypoxia, and that the additional Ca^<2+> influx causes irreversible change in the membrane of CAl neurons during prolonged hypoxia. For synaptic transmissions, IPSPs disappeared without change in EPSPs under hypoxia.
Study II: Minor brain injury was inflicted with a small needle one week before the production of incomplete brain ischemia in the mouse. A bilateral carotid clamp was applied for 60 min under pentobarbital or ketamine anesthesia, and the number of survivors in one week after the ischemic insult was compared with those in animals anesthetized only and a sham-oparated group. Survival rates following the brain ischemia induced during pentobarbital anesthesia were significantly higher in the brain injured group than in the other two groups. However, the improvement of the survival rates in mice with brain injury became insignificant when brain ischemia was imposed during ketamine anesthesia. The results suggest that the actions of certain factors or protective mechanisms against brain ischemia were developed by brain injury and that the brain injury-induced anti-ischemic activity is antagonized by ketamine and/or potentiated by barbiturate anesthesea. Less
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Report
(2 results)
Research Products
(18 results)
