Titlebook: New Aspects in the Treatment of Failing Heart; Hisakazu Yasuda (Emeritus Professor),Hideaki Kawag Conference proceedings 1992 Springer-Ver

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Mitochondrial DNA Mutations in Cardiomyopathy, 22 tRNAs required for translation of their mRNA, and two rRNA [1]. The mutation rate in mitochondrial DNA (mtDNA) is more than 10 times higher than that of nuclear DNA [2]. This is due to absence of introns, lack of DNA-binding proteins such as histones, simple DNA repair mechanism, and constant e

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Regulation of the Gs Protein in the Heartones and neurotransmitters that regulate the heart and vascular system have been shown to produce their effects by the activation of such proteins (1). Acetylcholine released by post?ganglionic parasympathetic (vagal) neurons and norepinephrine released at postganglionic sympathetic neurons are the

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Alterations in α-Adrenergic Receptors in Response to Myocardial Ischemia and their Role in Arrhythmohythmias during early myocardial ischemia [1–3]. There are at least two major mechanisms which underly the release of catecholamines during ischemia, the most prominent of which is local release from sympathetic nerve endings directly in the absence of any sympathetic neural activation [4]. In addit

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Enzyme-Specific Desensitization of Adenylyl Cyclase in Hypertrophied Heart in Monocrotaline-Treated results in pulmonary arterial hypertension, leading to a severe right ventricular hypertrophy and eventually to failure [1]. As reported in patients with heart failure caused by primary pulmonary hypertension, a chamber-specific decrease in the myocardial β-adrenoceptors was shown mostly in the fai

兒童

A Mechanism of Catecholamine Tolerance In Congestive Heart Failureiac dysfunction observed in CHF. However, CHF patients (or animals) share several similar features: reduced cardiac contractility, increased sympathetic nerve activity, and activation of several hormonal systems (e.g., renin-angiotensin system, vasopressin, and atrial natriuretic factor) to compensa