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Mammalian Heart (mammalian + heart)
Selected AbstractsSunao Tawara: A Father of Modern CardiologyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001KOZO SUMA SUMA, K.: Sunao Tawara: A Father of Modern Cardiology. Knowledge of the conduction system of the heart was greatly advanced by Tawara's work carried out in Aschoff's laboratory in Marburg at the beginning of this century. In his monograph, The Conduction System of the Mammalian Heart, published in 1906, Tawara indicated that the treelike structure of specific muscle fibers comprising the atrioventricular node, His bundle, bundle branches, and Purkinje fibers served as the pathway for atrioventricular conduction of excitation in the mammalian heart. From his own anatomic and histological findings of the conduction system, he assumed precisely that the conduction velocity of excitation in the system, except in the atrioventricular node, would be fast and that contraction as the result of excitation would take place at the various sites of the ventricles almost simultaneously. According to Tawara, a long pathway to each contracting unit and a fast conduction velocity of excitation would be a prerequisite for the effective contraction of the ventricles. Tawara's findings and assumptions provided Einthoven the theoretical basis for interpreting the electrocardiogram, resulting in rapid popularization of electrocardiography. This century has witnessed the rapid progress of cardiology, including cardiac pacing and its related sciences. This progress has its roots in the discovery of the conduction system and the development of electrocardiography that took place almost in the same period at the beginning of this century. Tawara's pioneering work on the conduction system still serves as an invaluable reference for basic and clinical research. [source] Origin and fate of cardiac mesenchymeDEVELOPMENTAL DYNAMICS, Issue 10 2008Brian S. Snarr Abstract The development of the embryonic heart is dependent upon the generation and incorporation of different mesenchymal subpopulations that derive from intra- and extra-cardiac sources, including the endocardium, epicardium, neural crest, and second heart field. Each of these populations plays a crucial role in cardiovascular development, in particular in the formation of the valvuloseptal apparatus. Notwithstanding shared mechanisms by which these cells are generated, their fate and function differ profoundly by their originating source. While most of our early insights into the origin and fate of the cardiac mesenchyme has come from experimental studies in avian model systems, recent advances in transgenic mouse technology has enhanced our ability to study these cell populations in the mammalian heart. In this article, we will review the current understanding of the role of cardiac mesenchyme in cardiac morphogenesis and discuss several new paradigms based on recent studies in the mouse. Developmental Dynamics 237:2804,2819, 2008. © 2008 Wiley-Liss, Inc. [source] Potential clinical relevance of the ,little brain' on the mammalian heartEXPERIMENTAL PHYSIOLOGY, Issue 2 2008J. A. Armour It is hypothetized that the heart possesses a nervous system intrinsic to it that represents the final relay station for the co-ordination of regional cardiac indices. This ,little brain' on the heart is comprised of spatially distributed sensory (afferent), interconnecting (local circuit) and motor (adrenergic and cholinergic efferent) neurones that communicate with others in intrathoracic extracardiac ganglia, all under the tonic influence of central neuronal command and circulating catecholamines. Neurones residing from the level of the heart to the insular cortex form temporally dependent reflexes that control overlapping, spatially determined cardiac indices. The emergent properties that most of its components display depend primarily on sensory transduction of the cardiovascular milieu. It is further hypothesized that the stochastic nature of such neuronal interactions represents a stabilizing feature that matches cardiac output to normal corporal blood flow demands. Thus, with regard to cardiac disease states, one must consider not only cardiac myocyte dysfunction but also the fact that components within this neuroaxis may interact abnormally to alter myocyte function. This review emphasizes the stochastic behaviour displayed by most peripheral cardiac neurones, which appears to be a consequence of their predominant cardiac chemosensory inputs, as well as their complex functional interconnectivity. Despite our limited understanding of the whole, current data indicate that the emergent properties displayed by most neurones comprising the cardiac neuroaxis will have to be taken into consideration when contemplating the targeting of its individual components if predictable, long-term therapeutic benefits are to accrue. [source] Calcium homeostasis and signaling in yeast cells and cardiac myocytesFEMS YEAST RESEARCH, Issue 8 2009Jiangjun Cui Abstract Calcium ions are the most ubiquitous and versatile signaling molecules in eukaryotic cells. Calcium homeostasis and signaling systems are crucial for both the normal growth of the budding yeast Saccharomyces cerevisiae and the intricate working of the mammalian heart. In this paper, we make a detailed comparison between the calcium homeostasis/signaling networks in yeast cells and those in mammalian cardiac myocytes. This comparison covers not only the components, structure and function of the networks but also includes existing knowledge on the measured and simulated network dynamics using mathematical models. Surprisingly, most of the factors known in the yeast calcium homeostasis/signaling network are conserved and operate similarly in mammalian cells, including cardiac myocytes. Moreover, the budding yeast S. cerevisiae is a simple organism that affords powerful genetic and genomic tools. Thus, exploring and understanding the calcium homeostasis/signaling system in yeast can provide a shortcut to help understand calcium homeostasis/signaling systems in mammalian cardiac myocytes. In turn, this knowledge can be used to help treat relevant human diseases such as pathological cardiac hypertrophy and heart failure. [source] Cardiomyocyte precursors and telocytes in epicardial stem cell niche: electron microscope imagesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2010Mihaela Gherghiceanu Abstract A highly heterogeneous population of stem and progenitor cells has been described by light immunohistochemistry in the mammalian adult heart, but the ultrastructural identity of cardiac stem cells remains unknown. Using electron microscopy, we demonstrate the presence of cells with stem features in the adult mouse heart. These putative cardiac stem cells are small (6,10 ,m), round cells, with an irregular shaped nucleus, large nucleolus, few endoplasmic reticulum cisternae and mitochondria, but numerous ribosomes. Stem cells located in the epicardial stem cell niche undergo mitosis and apoptosis. Cells with intermediate features between stem cells and cardiomyocyte progenitors have also been seen. Moreover, electron microscopy showed that cardiomyocyte progenitors were added to the peripheral working cardiomyocytes. Telocytes make a supportive interstitial network for stem cells and progenitors in the stem cell niche. This study enhances the hypothesis of a unique type of cardiac stem cell and progenitors in different stages of differentiation. In our opinion, stem cells, cardiomyocyte progenitors and telocytes sustain a continuous cardiac renewal process in the adult mammalian heart. [source] Natriuretic peptides in relation to the cardiac innervation and conduction systemMICROSCOPY RESEARCH AND TECHNIQUE, Issue 5 2002Magnus HanssonArticle first published online: 10 SEP 200 Abstract During the past two decades, the heart has been known to undergo endocrine action, harbouring peptides with hormonal activities. These, termed "atrial natriuretic peptide (ANP)," "brain natriuretic peptide (BNP)," and "C-type natriuretic peptide (CNP)," are polypeptides mainly produced in the cardiac myocardium, where they are released into the circulation, producing profound hypotensive effects due to their diuretic, natriuretic, and vascular dilatory properties. It is, furthermore, well established that cardiac disorders such as congestive heart failure and different forms of cardiomyopathy are combined with increased expression of ANP and BNP, leading to elevated levels of these peptides in the plasma. Besides the occurrence of natriuretic peptides (NPs) in the ordinary myocardium, the presence of ANP in the cardiac conduction system has been described. There is also evidence of ANP gene expression in nervous tissue such as the nodose ganglion and the superior cervical ganglion of the rat, ganglia known to be involved in the neuronal regulation of the heart. Furthermore, in the mammalian heart, ANP appears to affect the cardiac autonomic nervous system by sympathoinhibitory and vagoexcitatory actions. This article provides an overview of the relationship between the cardiac conduction system, the cardiac innervation and NPs in the mammalian heart and provides data for the concept that ANP is also involved in neuronal cardiac regulation. Microsc. Res. Tech. 58:378,386, 2002. © 2002 Wiley-Liss, Inc. [source] Sunao Tawara: A Father of Modern CardiologyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001KOZO SUMA SUMA, K.: Sunao Tawara: A Father of Modern Cardiology. Knowledge of the conduction system of the heart was greatly advanced by Tawara's work carried out in Aschoff's laboratory in Marburg at the beginning of this century. In his monograph, The Conduction System of the Mammalian Heart, published in 1906, Tawara indicated that the treelike structure of specific muscle fibers comprising the atrioventricular node, His bundle, bundle branches, and Purkinje fibers served as the pathway for atrioventricular conduction of excitation in the mammalian heart. From his own anatomic and histological findings of the conduction system, he assumed precisely that the conduction velocity of excitation in the system, except in the atrioventricular node, would be fast and that contraction as the result of excitation would take place at the various sites of the ventricles almost simultaneously. According to Tawara, a long pathway to each contracting unit and a fast conduction velocity of excitation would be a prerequisite for the effective contraction of the ventricles. Tawara's findings and assumptions provided Einthoven the theoretical basis for interpreting the electrocardiogram, resulting in rapid popularization of electrocardiography. This century has witnessed the rapid progress of cardiology, including cardiac pacing and its related sciences. This progress has its roots in the discovery of the conduction system and the development of electrocardiography that took place almost in the same period at the beginning of this century. Tawara's pioneering work on the conduction system still serves as an invaluable reference for basic and clinical research. [source] Expression pattern of neuronal and skeletal muscle voltage-gated Na+ channels in the developing mouse heartTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Volker Haufe In the mammalian heart, a variety of voltage-gated Na+ channel transcripts and proteins have been detected. However, little quantitative information is available on the abundance of each transcript during development, or the contribution of TTX-sensitive Na+ channels to the cardiac sodium current (INa). Using competitive and real-time RT-PCR we investigated the transcription of six Na+ channels (Nav1.1,Nav1.6) and the ,1 subunit during mouse heart development. Nav1.5 was predominantly expressed in the adult heart, whereas the splice variant Nav1.5a was the major Na+ channel isoform in embryonic hearts. The TTX-resistant Na+ channel transcripts (Nav1.5 and Nav1.5a) increased 1.7-fold during postnatal development. Transcripts encoding TTX-sensitive Na+ channels (Nav1.1,Nav1.4) and the ,1 subunit gradually increased up to fourfold from postnatal day (P)1 to P126, while the Nav1.6 transcript level remained low and constant over the same period. In adults, TTX-sensitive channel mRNA accounted for 30,40% of the channel pool in whole-heart preparations (Nav1.3 > Nav1.4 > Nav1.2 , Nav1.1 , Nav1.6), and 16% in mRNA from isolated cardiomyocytes (Nav1.4 > Nav1.3 > Nav1.2 > Nav1.1 > Nav1.6). Confocal immunofluorescence on ventricular myocytes suggested that Nav1.1 and Nav1.2 were localized at the intercalated disks and in the t tubules. Nav1.3 labelling predominantly produced a diffuse but strong intracellular signal. Nav1.6 fluorescence was detected only along the Z lines. Electrophysiological recordings showed that TTX-sensitive and TTX-resistant Na+ channels, respectively, accounted for 8% and 92% of the INa in adult ventricular cardiomyocytes. Our data suggest that neuronal and skeletal muscle Na+ channels contribute to the action potential of cardiomyocytes in the adult mammalian heart. [source] The signal transduction cascade regulating the expression of the gap junction protein connexin43 by ,-adrenoceptorsBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009A Salameh Background and purpose:, In mammalian heart, connexin43 (Cx43) represents the predominant connexin in the working myocardium. As the ,-adrenoceptor is involved in many cardiac diseases, we wanted to clarify the pathway by which ,-adrenoceptor stimulation may control Cx43 expression. Experimental approach:, Cultured neonatal rat cardiomyocytes were stimulated with isoprenaline. Cx43 expression as well as activation of p38 mitogen-activated protein kinase (MAPK), p42/44 MAPK, JUN NH2 -terminal kinase (JNK) and nuclear translocation of the transcription factors activator protein 1 (AP1) and CRE-binding protein (CREB) were investigated. Additionally, we assessed Cx43 expression and distribution in left ventricular biopsies from patients without any significant heart disease, and from patients with either congestive heart failure [dilated cardiomyopathy (DCM)] or hypertrophic cardiomyopathy (HCM). Key results:, Isoprenaline exposure caused about twofold up-regulation of Cx43 protein with a pEC50 of 7.92 ± 0.11, which was inhibited by propranolol, SB203580 (4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl)-1H-imidazole) (p38 inhibitor), PD98059 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one) (MAPK 1 kinase inhibitor) (Alexis Biochemicals, San Diego, CA, USA) or cyclosporin A. Similar findings were obtained for Cx43 mRNA. Furthermore, Cx43 up-regulation was accompanied by phosphorylation of p38, p42/44 and JNK, and by translocation of AP1 and CREB to the nucleus. Analysis of Cx43 protein and mRNA in ventricular biopsies revealed that in patients with DCM, Cx43 content was significantly lower, and in patients with HCM, Cx43 content was significantly higher, relative to patients without any cardiomyopathy. More importantly, Cx43 distribution also changed with more Cx43 being localized at the lateral border of the cardiomyocytes. Conclusion and implication:, ,-adrenoceptor stimulation up-regulated cardiac Cx43 expression via a protein kinase A and MAPK-regulated pathway, possibly involving AP1 and CREB. Cardiomyopathy altered Cx43 expression and distribution. [source] | |||||||||||||