| Project/Area Number |
10470163
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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 |
Circulatory organs internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
KODAMA Itsuo Nagoya Univ., Res. Inst. of Environ. Med., Professor, 環境医学研究所, 教授 (30124720)
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| Co-Investigator(Kenkyū-buntansha) |
SAKUMA Ichiro Nagoya Univ., Res. Inst. of Environ. Med., Professor, 大学院・工学系研究科, 助教授 (50178597)
HARUO Honjo Nagoya Univ., Res. Inst. Of Environ. Med., Associate Professor, 環境医学研究所, 助教授 (70262912)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1998: ¥5,800,000 (Direct Cost: ¥5,800,000)
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| Keywords | ventricular tachycardia / action potential / reentry / voltage-sensitive dye / DC shock / antiarrhythmic drug / electrophysiology / 多形性心室頻拍 / スパイラル型リエントリー / 活動電位光学計測 |
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| Research Abstract |
1. In this study, we investigated mechanisms underlying DC shock-induced polymorphic ventricular tachycardia (PVT) and effects of various drugs on PVT in rabbit hearts perfused in vitro.
2. Fluorescent action potential signals were recorded from 8-32 epicardial sites of ventricles stained with a voltage-sensitive dye (di-4-ANEPPS) with the use of our custom-built optical recording system. Stable optical signals with a high S/N ratio (>50dB) were routinely recorded with a small base-line drift of -3.6%/min.
3. Application of DC shocks (10-40V) during the repolarization phase of action potentials caused a prolongation of action potentials and an enhancement of spatial dispersion of ventricular repolarization, giving rise to an initiation of circuitous movement of excitation leading to PVT.
4. Biphasic shocks caused less dispersion of ventricular repolarization and lower incidence and shorter duration of PVT than monophasic shocks.
5. 10μM disopyramide prolonged ventricular action potentials
… More
with minimal effects on conduction velocity, whereas 30 μM disopyramide decreased significantly ventricular conduction velocity. In the presence of 10μM disopyramide, vulnerability to PVT induction by DC shock was slightly reduced. In contrast, in the presence of 30μM disopyramide, vulnerability to PVT was greatly increased and induced PVT showed much longer perpetuation than controls. E-4031 (0.1μM) caused a reverse-frequency dependent prolongation of ventricular action potentials and a marked decrease in vulnerability to PVT with shorter perpetuation.
6. Stimulation of β adorenergic receptor by isoproterenol (0.1μM) resulted in a shortening of action potentials with considerable regional differences. In the presence of isoproterenol, PVT showed longer perpetuation than controls.
7. In conclusion, DC shocks initiate circuitous movement of excitation underlying PVT through an enhancement of spatial inhomogeneity of ventricular repolarization, and drug-induced in ADP dispersion may facilitate and exaggerate DC shock-induced reentrant tachyarrhythmias. Less
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