| Project/Area Number |
04670536
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 | Shimane Medical University |
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Principal Investigator |
HONDA Masaaki (1993-1994) Shinema Medical University, Department of Internal Medicine, Assistant Professor, 医学部, 講師 (90127530)
森山 勝利 (1992) 島根医科大学, 医学部, 教授 (10034919)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Koichi Shimane Medical University, Department of Internal Medicine, Instructor, 医学部, 助手 (00252924)
ISHINAGA Yuji Shimane Medical University, Department of Internal Medicine, Instructor, 医学部, 助手 (70243433)
MORIOKA Shigefumi Shimane Medical University, Department of Internal Medicine, Associate Professor, 医学部, 助教授 (00157877)
本田 正明 島根医科大学, 医学部, 講師 (90127530)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Heart failure / Calcium Transients / Monocrotaline / Cardiac hypertrophy / Heart rate dependency / heart failure / calcium transients / adrenergic response / single myocytes |
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| Research Abstract |
Objectives & Methods : Intarcellular free calcium ion plays important roles in excitation-contraction coupling in cardiac myocytes, thereby regulating cardiac function. Recent studies of ours and others have revealed abnormal calcium handling in failing heart. To examine characteristics of calcium handling in failing heart, we used monocrotaline-induced right ventricular hypertrophy model with heart failure. After cardiac myocytes were separated from RV by Langendorff apparatus, Fura-2/AM was leaed. Calcium transients (Ca-T) were measured by changing stimulatory frequency from 0.5Hz to 5Hz.
Results : Peak ratio (PR) and resting ratio (PR) of Ca-T in control normal heart increased with the increase in stimulatory frequency, with net increase in amplirude (PR-PR) . PR and PR of Ca-T in failing heart also increased as the stimulatory frequency increased. However, amplitude of Ca-T in failing heart decreased with the increase in stimulatory frequency. Remarkable increase in RR with no amplitude was observed when the myocytes from failing heart were stimulated at 5 Hz. These changes in Ca-T in failing heart correlated well with the severity of heart failure. The changes in Ca-T with changes in stimulatory frequency in normal and failing heart were reversible. Conclusions : Ca-T,especially, RR and amplitude, in failing heart alter with increase in stimulatory frequency. That is intracellular free calcium release and reuptake mechanisms were disturbed remarkably with the increase in heart rate in failing heart, which may result in further systolic and diastolic dysfunction. Although exact mechanism for heart rate-dependent abnormalities should be elucidated, heart rate control in failing heart is important to maintain and/or improve cardiac function in failing heart.
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