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Titlebook: Inotropic Stimulation and Myocardial Energetics; Hj. Just,Ch. Holubarsch,H. Scholz Conference proceedings 1989 Springer-Verlag Berlin Heid

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書(shū)目名稱Inotropic Stimulation and Myocardial Energetics
編輯Hj. Just,Ch. Holubarsch,H. Scholz
視頻videohttp://file.papertrans.cn/468/467644/467644.mp4
圖書(shū)封面Titlebook: Inotropic Stimulation and Myocardial Energetics;  Hj. Just,Ch. Holubarsch,H. Scholz Conference proceedings 1989 Springer-Verlag Berlin Heid
描述Inotropic stimulation of the myocardium, as well as vasodilation and diuresis as essential principles in the treatment of congestive heart failure have recently met with considerable criticism and reevaluation. It is generally agreed that unloading of the heart, either through vasodilation and/or diuresis, improves the working conditions of the dilated, failing heart. It reduces myocar- dial oxygen consumption through reduction of chamber radius and, thereby, wall tension as the major determinants of myocardial oxygen consumption. Inotropic stimulation, quite in contrast, does not conserve oxygen. It rather consumes energy and that may be disadvantageous in situations of compromised oxygen supply and energy metabolism of the working myocardium. However, under conditions of suf- ficient oxygen supply and metabolic support inotropic stimulation may bring about in- creased pumping and subsequent improvement of myocardial failure. In recent years it could convincingly be demonstrated that vasodilation leads to symp- tomatic improvement of congestive heart failure, improvement of exercise tolerance, and it prolongs life - especially in the case of ACE-inhibitors and the combination of h
出版日期Conference proceedings 1989
關(guān)鍵詞Hydra; arrhythmia; heart; heart failure; metabolism
版次1
doihttps://doi.org/10.1007/978-3-662-07908-9
isbn_softcover978-3-662-07910-2
isbn_ebook978-3-662-07908-9
copyrightSpringer-Verlag Berlin Heidelberg 1989
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978-3-662-07910-2Springer-Verlag Berlin Heidelberg 1989
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Introduction: Mechanisms of positive inotropic effectsthe action potential induced by K. channel-inhibiting agents such as 4-amino-pyridine may increase the myoplasmic Ca. concentration by a prolongation of the slow Ca. inward current; 6) An increased Ca. sensitivity of the contractile proteins has been demonstrated for a number of compounds in vitro;
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Genetic and non-genetic control of myocardial calciumypertrophy the amount of calcium cycled is unchanged while the rate is increased. In the pressure overload hearts there is a decrease in sarcoplasmic reticular (SR) Ca. ATPase, whereas in the thyrotoxic preparations the message is increased. The change in the rate of calcium uptake in pressure overl
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Regulation of force and intracellular calcium transients by cyclic AMP generated by forskolin, MDL 1of myofibrils by cyclic AMP generated by .-adrenoceptor stimulation. Carbachol, which did not affect significantly the basal force and cyclic AMP levels, lowered the cyclic AMP levels elevated previously by forskolin, MDL 17,043 or isoprenaline in the isolated dog ventricular trabeculae. It antagoni
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