112 THE AGE DEPENDENCY OF MYOCARDIAL EXCITATION CONTRACTION COUPLING

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The impact of age on cardiac excitation-contraction coupling

1. Cardiovascular diseases most commonly occur in the elderly and are a frequent cause of disability or death. However, the effect of age itself on cardiac function is not well understood. 2. Studies in both human and animal hearts indicate that contractile function is unaffected by age while at rest. However, the ability to increase cardiac contractile force during strenuous activities such as...

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Altered Excitation-Contraction Coupling

Heart Failure After Myocardial Infarction : Altered Excitation-Contraction Coupling Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2001 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/hc3201.092285 2001;104:688-693 Circulation. http://circ.ahajournals.org/content/10...

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Excitation-Contraction Coupling

Previous studies have demonstrated that the ability of (.adrenergic receptor (.BAR) stimulation to increase cardiac contractility declines with aging. In the present study, the control mechanisms of excitation-contraction (EC) coupling, including calcium current (Ice), cytosolic Ca2" (Ca?') transient and contraction in response to BAR stimulation were investigated in ventricular myocytes isolat...

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Heart failure after myocardial infarction: altered excitation-contraction coupling.

BACKGROUND Heart failure (HF) frequently follows the occurrence of myocardial infarction (MI). Questions about how HF develops and what cellular defects contribute to this dysfunction led to this study. Methods and Results-- MI was induced in rats by coronary artery ligation. Clinical examination of the post-MI (PMI) surviving animals indicated that they were in overt HF by all measures. Cellul...

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Uncoupling protein-2 modulates myocardial excitation-contraction coupling.

RATIONALE Uncoupling protein (UCP)2 is a mitochondrial inner membrane protein that is expressed in mammalian myocardium under normal conditions and upregulated in pathological states such as heart failure. UCP2 is thought to protect cardiomyocytes against oxidative stress by dissipating the mitochondrial proton gradient and mitochondrial membrane potential (DeltaPsi(m)), thereby reducing mitoch...

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ژورنال

عنوان ژورنال: Pediatric Research

سال: 1985

ISSN: 0031-3998,1530-0447

DOI: 10.1203/00006450-198504000-00142