Titlebook: Cellular and Molecular Alterations in the Failing Human Heart; G. Hasenfuss,Ch. Holubarsch,N. R. Alpert Conference proceedings 1992 Dr. Di

Angioplasty

https://doi.org/10.1007/978-3-540-77058-9 whereas at higher stimulation rates force declined again. These results indicate that (1.) alterations of the force-frequency relationship in the failing human heart depend on the underlying cardiac disease and/or the time-course of the disease, and (2.) an increase in the extracellular Ca.-concent

aneurysm

Receptor systems in the non-failing human heart the cardiac .-adrenoceptor-G.-protein-adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility..On the other hand, at least three receptor systems acting through inhibition of cAMP formation (G.-protein coupled receptors) exist in the human heart: muscarinic

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Changes in the receptor-G protein-adenylyl cyclase system in heart failure from various types of hean function may be the basis for .-receptor uncoupling in IDC and ISCDC, whereas in PPH, this phenomenon may result from altered adenylyl cyclase function. Catalytic subunit activity of adenylyl cyclase is decreased in order of increasing pulmonary hypertension in right-ventricular preparations from

legitimate

Quantification of Giα-proteins in the failing and nonfailing human myocardiumdilated cardiomyopathy and 48% in ischemic cardiomyopathy, although pertussis toxin substrates were only increased by 40% in dilated cardiomyopathy and no change was observed in ischemic cardiomyopathy. In cardiomyopathy tissue, an inverse relationship was observed between the increase of G. and the

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GIDDY

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Spina-Bifida

Structural and functional diversity of human ventricular myosin Because the two bands were detected also in normal hearts of large mammals, the existence of V./V. cannot be diagnostic of diseased heart. However, the V./V. ratio was influenced by the hemodynamic load, whereby the fast migrating band (V.) increased with the diastolic and systolic load. Because a

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Troponin T isoform expression in the normal and failing human left ventricle: a correlation with myoofibrillar percentage of total troponin T comprised of TnT.. In that heart failure in these transplant patients had multiple bases, we propose that rather than a cause of heart failure, the disease-associated changes in troponin T isoform expression are an adaptation to abnormal myocardial function.