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Titlebook: Recent Progress in Failing Heart Syndrome; Shigetake Sasayama (Professor of Medicine),Hiroyuk Book 1991 Springer-Verlag Tokyo 1991 adaptat

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發(fā)表于 2025-3-21 16:23:48 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Recent Progress in Failing Heart Syndrome
編輯Shigetake Sasayama (Professor of Medicine),Hiroyuk
視頻videohttp://file.papertrans.cn/824/823304/823304.mp4
圖書封面Titlebook: Recent Progress in Failing Heart Syndrome;  Shigetake Sasayama (Professor of Medicine),Hiroyuk Book 1991 Springer-Verlag Tokyo 1991 adaptat
描述Heart failure is a syndrome caused by a heart dysfunction that leads to insuf- ficient blood in the peripheral tissues for their metabolic demands. This syn- drome still remains an obscure clinical entity and even its definition is disputed. It has become increasingly apparent that heart failure may relate not only to cardiac dysfunction but also to other physiological alterations involved in the maintenance of circulatory homeostasis. In 1988, the Japanese Circulation Society organized a three-year project for research on heart failure. The research group consisted of ten investigators, all relatively young but well recognized internationally for their research accomplishments. This book represents a compilation of the achievements by this group during the past three years which have led to new insights into the pathophysiologic mechanisms of heart failure, and diagnosis, evaluation and treatment of this syndrome. Contents include research into the cellular biology of congestive heart failure, and a framework of pressure-volume relationships enabling assessment of ventricular contraction energetics or coupling of ventricular properties and arterial load. This conceptual framework
出版日期Book 1991
關(guān)鍵詞adaptation; artery; biology; circulation; heart; heart failure; myocardial infarction; physiology; stroke
版次1
doihttps://doi.org/10.1007/978-4-431-67955-4
isbn_softcover978-4-431-68019-2
isbn_ebook978-4-431-67955-4
copyrightSpringer-Verlag Tokyo 1991
The information of publication is updating

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Book 1991is syn- drome still remains an obscure clinical entity and even its definition is disputed. It has become increasingly apparent that heart failure may relate not only to cardiac dysfunction but also to other physiological alterations involved in the maintenance of circulatory homeostasis. In 1988, t
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Molecular Basis for Cardiac Adaptation to Overload,ituents. We demonstrated the distribution of two types of cardiac myosin heavy chains (HCα and HCβ) in the human heart using monoclonal antibodies. The ventricle comprised mainly of HCβ has low ATPase activity, whereas the atrium was predominantly composed of HCα and has high ATPase activity. We als
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Cardiac Oxygen Costs of Contractility (Emax) and Mechanical Energy (PVA): New Key Concepts in Cardim are summarized. We have proposed that the contractile state of the ventricle can be quantified by the end-systolic ventricular maximum volume elastance (E.) and that the total mechanical energy of ventricular contraction can be quantified by the systolic pressure-volume area (PVA). E. is the slope
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