| Project/Area Number |
25861401
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ミトコンドリア / 鎮静薬 / 敗血症性脳症 / プロポフォール / デクスメデトミジン / 呼吸鎖 / 麻酔薬 / 脳内ミトコンドリア / Ca代謝 / 麻酔薬の影響 |
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| Outline of Final Research Achievements |
We acknowledged that propofol affected the induced increase in the permeability of mitochondrial membrane and the respiration chain by its dosage. The possibility that might induce the cell death of mitochondria and the cessation of respiration chain was suggested. In comparison to it, we did not acknowledge that sevoflurane, midazolam and dexmedetomidine affected it in spite of their dosages. In addition, propofol, sevoflurane, and midazolam suppressed the ability which mitochondria took in calcium. On the other hand, we did not acknowledge that dexmedetomidine affected it. We aimed at analyzing the pathologic condition of septic encephalopathy from the viewpoint of mitochondria but the research findings led to the concerned conclusion that various tranquilizers affected the brain mitochondrial functions as the first stage of analysis in the mechanism of septic encephalopathy which tranquilizers developed delirium.
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