| Project/Area Number |
17591608
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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 | Hirosaki University |
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Principal Investigator |
KUSHIKATA Tetsuya Hirosaki University, Hirosaki University, University Hospital, Lecturer (80250603)
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| Co-Investigator(Kenkyū-buntansha) |
HIROTA Kazuyoshi Hirosaki University, Graduate School of Medicine, Professor (20238413)
KUDO Mihoko Hirosaki University, Graduate School of Medicine, Assistant Professor (30003411)
YOSHIDA Hitoshi Hirosaki University, University Hospital, Assistant Professor (00374843)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | General anesthetics / Sleep / EEG / Rat / Cytokine |
|---|
| Research Abstract |
Anesthesia affected sleep wakefulness for around 1 week. For example, ketamine increased non rapid eye movement sleep (NREMS) transiently then decreased it. Conversely REM sleep was increased for 1 week as mirror image to NREMS. On the other hand, pentobarbital did not increased NREM apparently. We also measured several cytokine such as IL-1 beta, TNF alpha, IL-2, IL-4 and IL-10 that are considered sleep-related endogenous substance. Ketamine (100 mg/kg) increased IL-1 beta in the rat hypothalamus. For investigate of this meaning, we studied brain noradrenergic neurons and cytokine relationship because these sleep-related endogenous substance activate brain noradrenergic neuron and the neuron is responsible sleep-wakefulness, pain, and autonomic nervous system that are involved in process of general anesthesia. Indeed ketamine anesthesia time was increased in the rats treated with DSP-4, a specific toxin of the noradrenergic neuron.
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