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

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https://doi.org/10.1007/978-3-540-76890-6d cell was less able to buffer the changes in the intracellular calcium, thus providing a biological basis for the arrhythmogenicity of the hypertrophied heart. These various modifications may provide a new key for future pharmaceutical research.

BOOST

蛤肉

時代錯誤

Cardiovascular cyclic nucleotide phosphodiesterases and their role in regulating cardiovascular func diseases. More potent selective inhibitors of the cGMP-PDE isozyme are needed to determine whether these pharmacological potentiators of EDRF and ANP will be useful in the therapy of angina, hypertension or heart failure.

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圣歌

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Eine allgemeine Konvergenztheorie,n 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

HALO

https://doi.org/10.1007/978-3-540-76790-9dilated 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