| Project/Area Number |
14571417
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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 | Akita University |
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Principal Investigator |
NISHIKAWA Toshiaki Akita University, School of Medicine, Professor, 医学部, 教授 (50156048)
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| Co-Investigator(Kenkyū-buntansha) |
GOYAGI Toru Akita University, School of Medicine, Assistant professor, 医学部, 講師 (30302277)
KIMURA Tetsu Akita University, School of Medicine, Instructor, 医学部, 助手 (00312702)
TANAKA Makoto Akita University, School of Medicine, Associate Professor, 医学部, 助教授 (50236634)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | forebrain ischemia / neuroprotect effect / dexmedetomedine / lidocaine / α_2アゴニスト |
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| Research Abstract |
We investigated whether coadministration of lidocaine and dexmedetomidine would reduce brain injury following transient forebrain ischemia in rats to a greater extent than either drug alone.
Materials and Methods : Adult male Sprague-Dawley rats *were anesthetized with halothane to maintain normocapnia and normoxia. Rats received subcutaneous injection of saline 1 ml/kg, dexmedetomidine 3 mg/kg, lidocaine 10 mg/kg, or dexmedetomidine 3 mg/kg plus lidocaine 10 mg/kg. Thirty min after the drug injection, forebrain ischemia was induced by hemorrhagic hypotension and occlusion of the bilateral carotid arteries, and was confirmed by isoelectric EEG. At the end of 10-min ischemia, rats were reperfused. The same dose of drug was administered 3, 24, and 48 hours after ischemia. Neurological examination was done at 1, 2 and 7 days after ischemia. Seven days after ischemia, the brain was stained with hematoxylin and eosin. We counted ischemic cells in the CA1 and CA3 hippocampal regions, striatum and cerebral cortex. Also we measured glutamate and norepinephrine concentration in hopocampal CA1.
Results : As compared with saline-treated rats, rats receiving dexmedetomidine plus lidocaine showed less neurological deficit scores at 24 and 48 hours after ischemia, and had less ischemic cells in the CA1 region. Administration of dexmedetomidine plus lidocaine did not alter the area under the glutamate concentration curve and norepinephrine concentration during ischemia compared with saline-treated rats.
Conclusion : Our results suggest coadministration of lidocaine and dexmedetomidine reduce neurological deficit score without alteration of glutamate and norepinphrine concentration during forebrain ischemia.
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