| Project/Area Number |
13470322
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Nagasaki University |
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Principal Investigator |
SUMIKAWA Koji Nagasaki University, Graduate School of Biomedical Science, Professor, 大学院・医歯薬学総合研究科, 教授 (60028660)
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| Co-Investigator(Kenkyū-buntansha) |
HARA Tetsuya Nagasaki University, University Hospital of Medicine and Dentistry, Assistant professor, 医学部・歯学部附属病院, 講師 (50304952)
CHO Sungsam Nagasaki University, University Hospital of Medicine and Dentistry, Research Associate, 医学部・歯学部附属病院, 助手 (90325655)
MIYOSHI Hiroshi Nagasaki University, University Hospital of Medicine and Dentistry, Research Associate, 医学部・歯学部附属病院, 助手 (90332858)
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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 |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2003: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2001: ¥6,500,000 (Direct Cost: ¥6,500,000)
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| Keywords | myocardial ischemia / myocardial stunning / heart failure / coronary circulation / myocardial portection / contractile function / preconditioning / anesthetics / 虚血再灌流障害 / プレコンディショニング / プロポフォール / 交感神経β作動薬 / 微小塞栓 / デキサメデトミジン / 低酸素症 / Na^+ / Ca^<++>交換機構阻害薬 / 交感神経α_2作動薬 / KB-R7943 / 心筋 / スタニング / 吸入麻酔薬 / プロテインキナーゼC |
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| Research Abstract |
This study was carried out to investigate the mechanisms of myocardial stunning and to establish the pharmacological therapeutic method for myocardial stunning using the computer-based cardiovascular measurement system including the analysis of left ventricular pressure-volume relationship.
We investigated the hemodynamic and cardioprotective effects of sevoflurane or KB-R7943, a Na^+/Ca^<2+> exchanger inhibitor, on myocardial stunning in dogs. Sevoflurane has a cardioprotective effect mediated through activation of mitochondrial KATP channels and independent of coronary blood flow or reduction in cardiac work. KB-R7943 improves myocardial contractile dysfunction after ischemia-reperfusion in a dose-dependent, manner, and has no effect on coronary and systemic hemodynamics. We investigated the effects of propofol on myocardial contractility and oxygen balance in acute ischemic myocardium, using coronary microembolization model in dogs. Propofol causes a greater decrease in the contracti
… More
lity of acute ischemic myocardium as compared with normal myocardium, and oxygen imbalance is not involved in the mechanism of this propofol's action.
We demonstrated that overexpression of Glutaredoxin protected myocardium from hydrogen peroxide-induced apoptosis by regulating the redox state of Akt. Glutaredoxin plays an important role in protecting myocardium from oxidative stress.
We investigated the hemodynamic actions of dantrolene during propofol anesthesia. Dantrolene reverses the hypotensive action produced by propofol and causes an increase in coronary blood flow with a decrease in coronary vascular resistance. We investigated the effects of dexmedetomidine and propofol on the response of heart rate to intravenous isoproterenol. Dexmedetomidine but not propofol enhances the heart rate response to the continuous intravenous infusion of isoproterenol. We investigated the interaction of MCI-154, a calcium sensitizer, and isoflurane on myocardial contractility in chronically instrumented dogs after pharmacological autonomic nervous system activity blockade. MCI-154 increases myocardial contractility and decreases coronary vascular resistance without changing calculated myocardial oxygen consumption during both the conscious state and isoflurane anesthesia. Less
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