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Titlebook: Cardiac Adaptation in Heart Failure; Risks due to myocard J. Holtz,H. Drexler,H. Just Conference proceedings 1992 Dr. Dietrich Steinkopff V

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書(shū)目名稱(chēng)Cardiac Adaptation in Heart Failure
副標(biāo)題Risks due to myocard
編輯J. Holtz,H. Drexler,H. Just
視頻videohttp://file.papertrans.cn/222/221711/221711.mp4
圖書(shū)封面Titlebook: Cardiac Adaptation in Heart Failure; Risks due to myocard J. Holtz,H. Drexler,H. Just Conference proceedings 1992 Dr. Dietrich Steinkopff V
描述Traditionally, cardiac hypertrophy is regarded as an adaptation of the heart to permanent mechanical overload. Regardless of the fact that many different and often unknown primary causes can result in heart failure, mechanical overload and myocardial hypertrophy is found in almost all forms of manifest chronic heart failure (apart from failure due to extramyocardial hindrances to inflow or to relaxation). However, the reactive enlargement of myocardial mass in response to an enhanced hemodynamic burden appears to be a double-edged sword. Obviously, the hypertrophy helps to reduce the enhanced ventricular wall stress in heart failure by adding contractile units to the overdistended chamber wall. However, in recent years it became clear that this adaptive hypertrophic process is rather complex and may include problematic facets. The adaptive hypertrophy includes proliferation of the nonmyocyte cardiac cells as well as substantial alterations in the phenotype of the growing myocytes due to differential changes in gene expression.
出版日期Conference proceedings 1992
關(guān)鍵詞adaptation; arrhythmia; cells; endothelium; heart; heart failure; tissue
版次1
doihttps://doi.org/10.1007/978-3-642-72477-0
isbn_softcover978-3-642-72479-4
isbn_ebook978-3-642-72477-0
copyrightDr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt 1992
The information of publication is updating

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Michael J. Grimble,Pawe? Majeckitive failure. Catecholamines have long been implicated in the pathogenesis of myocardial hypertrophy, however, it is very difficult to sort out catecholamine mechanisms in vivo. We have developed a cell-culture model which excludes hemodynamic effects and allows the assignment of receptor specificit
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Michael J. Grimble,Pawe? Majeckiin a precise developmental and spatial program and are up-regulated, in the adult heart, by ischemia or a hemodynamic burden. The accumulation of trophic factors after aortic banding supports the hypothesis that autocrine or paracrine pathways might function to mediate, in part, the consequences of
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https://doi.org/10.1007/3-540-07945-9rdial contractile behaviour and cardiac pump function in a novel manner, mainly by influencing the duration of contraction and the onset of relaxation but without major effect on early systolic contractile characteristics. These effects are mediated by the release of at least two diffusible substanc
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S. P. Lin,W. R. C. Phillips,D. T. Valentineling dilated cardio-myopathic hearts at a stimulation rate of 60 beats per minute (37°C). This frequency was chosen because analysis of the force-frequency relation showed significant differences in isometric force between failing and nonfailing human myocardium at 60 beats per minute and at higher
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https://doi.org/10.1007/978-3-642-85084-4ly within and among cells. The SR can also generate spontaneous Ca. oscillations (S-CaOs), i.e., not triggered by sarcolemmal depolarization. The local increase in Ca. due to S-CaOs is equivalent to that induced by an AP. Heterogeneity of diastolic Ca. caused by asynchronous S-CaOs among cells withi
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