| Project/Area Number |
16591563
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Juntendo University |
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Principal Investigator |
NISHIMURA Kinya Juntendo University, Anesthesiology, associate Professor, 医学部, 助教授 (80164581)
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| Co-Investigator(Kenkyū-buntansha) |
WARABI Kengo Juntendo University, Anesthesiology, assistant professor, 医学部, 講師 (30311989)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | cerebral ischemia / patch clamp / volatile anesthetics / resting potential / GABA receptor / 発火パターン / bicuculline / 虚血耐性 / Patch clamp / マウス線条体 / 虚血耐性獲得現象 |
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| Research Abstract |
General anesthetics are known to reduce neuronal death caused by focal cerebral ischemia in rodents and by in vitro ischemia in cultured neurons and brains slices. In the present study, we investigated the cellular mechanisms underlying the neuroprotective action of volatile anesthetics in an ischemic brain slice preparation. In vitro ischemia of the identified striatal neuronal subtypes in a slice preparation of the mouse striatum (C57BL/6J) was induced by oxygen and glucose deprivation. Whole cell patch clamp recording was made in a current-clamp mode. We investigated the electrophysiological influence of volatile anesthetics utilizing intracellular current-clamp recording obtained from striatal neurons.
We found that in vitro ischemia invariably caused an increase of RP. This increase of RP was fully reversible by administering oxygen + glucose if given no later than 4.5 min. from the start point of ischemia (brief period of ischemia). However, the longer ischemia (oxygen + glucose given after 5 min) caused irreversible changes in most cases. In cases with administered volatile anesthetics, the ratio of reversible cases notably increased compared with the control group (=without volatile anesthetics). And, this increase was inhibited by the treatment with BMI.
Isoflurane and Sevoflurane may reduce the severity of key deleterious pathophysiologic events in an in vitro model of simulated cerebral ischemia. It was proved to prevent irreversible depolarization caused by simulated cerebral ischemia, although this neuroprotective effect does not seem strong. Cerebroportective effect could be expected from the volatile anesthetics administration.
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