| Project/Area Number |
06304030
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
TOYAMA Junji Nagoya Univ., Res.Inst.of Environ.Med., Professor, 環境医学研究所, 教授 (20023658)
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| Co-Investigator(Kenkyū-buntansha) |
TOMOIKE Hitonobu Yamagata Univ., School of Medicine, Professor, 医学部, 教授 (90112333)
INOUE Toshimichi Osaka Univ., School of Medicine, Professor, 医学部, 教授 (30028401)
MASHIMA Saburo Showa Univ., School of Medicine, Professor, 医学部, 教授 (30010333)
SAWANOBORI Tohru Tokyo Med.& Dental Univ., Medical Res.Inst., Associate Professor, 難治疾患研究所, 助教授 (00014217)
KIYOSUE Tatsuto Oita Medical Univ., Dept.of Physiology, Assistant Professor, 医学部, 助手 (90128348)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1994: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | re-entry of excitation / ischemia and K^+ accumulation / inhomogeneous excitability / modulation of ventricular repolarization / 致死性不整脈 / 心室細動 / 興奮伝導異方向性 / Kチャネルブロッカー / 電気ショック / 細胞間結合 |
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| Research Abstract |
This study was aimed to investigate the mechanisms of life-threatening ventricular tachyarrhythmias complicated with the acute and chronic phase of ischemia, and to find clues to develop pharmacologic and non-pharmacologic treatments for such arrhythmias.
In acute ischemia, potassium ion (K^+) was released from ATP-depleted myocytes by opening the ATP-dependent potassium channel and inhibition of Na-K pump, and was thus accumulated in the extracellular space. Such K^+ accumulation was not homogeneous but dependent on the severity of the ischemia, thereby leading to re-entrant arrhythmias caused by inhomogeneous depression of excitability and conductivity in the ischmic region. Administration of Mg ion or potassium channel opener could prevent such ventricular arrhythmias experimentally, but a further study should be done before clinical application.
In the chronic phase of ischemia, inhomogeneities of excitiation couduction were developed through remodelings of failing heart such as healing and/or apoptotic processes of muscle fibers in association with reactive proliferation of connective fibers. Thus, such complicated processes and reactions of the cardiac tissue shoud be taken into account in order to develop new pharmacological and non-pharmacological treatments for ventricular arrhythmias in the chronic phase of ischemia.
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