| Project/Area Number |
13671394
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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 |
Thoracic surgery
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| Research Institution | Kochi University |
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Principal Investigator |
NONAMI Yoshiki Kochi University, Faculty of Medicine, Assistant professor, 医学部附属病院, 講師 (20164717)
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| Co-Investigator(Kenkyū-buntansha) |
SASAGURI Sirou Kochi University, Faculty of Medicine, Professor, 医学部, 教授 (60196186)
HAMASATO Sinzi Kochi University, Faculty of Medicine, Assistant, 医学部, 助手 (60228533)
園部 宏 高知医科大学, 医学部, 助教授 (20145121)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | cardiomyocytes / endothels / L-Arginine / nitric oxide |
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| Research Abstract |
Protective effects of L-arginine were evaluated in a cardiomyocytes and endothels got from rats model of low-volume anoxia and re-oxygenation. Cell cultures were subjected to 90 min of low-volume anoxia and 30 min of re-oxygenation. L-Arginine (0-0.5 mM) was administered during the pre-anoxic period or the re-oxygenation phase. Nitric oxide (NO) production, NO synthase (NOS) activity, cGMP levels, and cellular injury were assessed. To evaluate the effects of the L-arginine on cell signaling, the effects of the NOS antagonist NG-nitro-L-arginine methyl ester (L-NAME), No donor S-nitroso-N-acetyl-penicillamine (SNAP), guanylate cyclase inhibitor methylene blue, cGMP analog 8-bromo-cGMP were examined. This data indicate that low-volume anoxia and re-oxygenation might increase NOS activity and facilitated the conversion of L-arginine to NO, which provided protection against cellular injury in a dose-dependent fashion. In addition, the cardioprotective effects of L-arginine were achived by the activation of guanylate cyclase, leading to increased cGMP levels in rat heart cells. This action involves a glibenclamide-sensitive, NO-cGMP-dependent pathway.
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