| Project/Area Number |
62570392
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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 | Osaka University |
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Principal Investigator |
HORI Masatsugu Osaka University School of Medicine research assistant, 医学部, 助手 (20124779)
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| Co-Investigator(Kenkyū-buntansha) |
UEMATSU Masaaki Osaka University Medical Hospital Resident, 医学部附属病院, 医員
ISHIHARA Ken Osaka University Medical Hospital Resident, 医学部附属病院, 医員 (20304610)
ONISHI Shunzo College of Biomedical Technology of Osaka University Professor, 医療短期大学, 教授 (00028367)
INOUE Michitoshi Osaka University Medical Hospital Professor, 医学部附属病院, 教授 (30028401)
是恒 之宏 大阪大学, 医学部付属病院, 医員
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | congestive heart failure / sympathetic nerve activity / catecholamine / beta-adrenergic receptor down-regulation / down-regulation / 遷延性心筋虚血 / β受容体 / 微小循環障害 |
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| Research Abstract |
It is well known that inotropic response of the beta-adrenoceptor stimulation is markedly depressed in congestive heart failure. This phenomenon is due to the down-regulation of beta-adrenergic receptors and abnormalities of the subcellular signal transduction system. However, in the pre-failure stage, cardiac beta-adrenoceptors are often increased. These observations may support the view that beta-adrenoceptor changes play an important role in manifestation of the heart failure. To test this hypothesis, we studied the changes in cardiac function and beta-adrenoceptor density in dogs 7 days after recovery from acute myocardial ischemia produced by intracoronary microembolization (15 or 25 m in diam). Myocardial norepinephrine content was depleted, but the number of betaadrenergic receptors was increased, and thus basal cardiac function was restored to normal. However, inotropic response to intravenous administration of forskolin was significantly depressed whereas the response to isoproterenol was apparently normal. These results indicate that an increase in beta-adrenergic receptors in ischemic cardiomyopathy may compensate the impaired subcellular signal transduction of beta-receptors. To verify this idea, increased beta-adrenergic receptors were imposed to be down-regulated by sustained infusion of isoproterenol. As expected, overt heart failure became manifest following the down-regulation of betaadrenoceptors. These results indicate that beta-adrenoceptor change plays a major role in compensation and expression of heart failure.
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