1,721,257 research outputs found

    Embryology of congenital ventriculo-coronary communications: a study on quail-chick chimeras

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    Ventriculo-coronary arterial communications are rare congenital heart defects which have been explained traditionally on the basis of abnormal persistence of such communications found in the normal developing heart. Recent studies, however, have suggested that these embryonic communications might be an incidental finding rather than a normal feature. Thus, it has been suggested that congenital ventriculo-coronary communications do not represent remnants of normal embryonic vessels, but rather represent acquired lesions. In the present study, hearts were constructed in embryonic chicks in which the coronary vasculature was almost completely derived from a quail-donor. After immunohistochemical staining of the quail-derived coronary endothelium, chimeric hearts were analysed with respect to the presence of embryonic ventriculo-coronary communications, and with respect to the origin of these structures from either coronary arteries or endocardium. The results demonstrate the normal presence of ventriculo-coronary communications in avian embryonic hearts. They show, furthermore, that these structures are of coronary endothelial origin. The findings are in accord with the traditional view on the pathogenesis of congenital ventriculo-coronary communications. The roles of elevated ventricular pressure, abnormal remodelling of the developing myocardium, and of abnormal growth of the coronary vasculature are discussed relative to the pathogenesis of congenital ventriculo-coronary communications

    Ontogenetic development of the helical heart: concepts and facts

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    The structural and functional organization of the ventricular myocardial mass is a controversial matter that cannot be resolved by anatomical studies alone. Therefore, other approaches such as investigations of the ontogenetic development of the ventricular myocardium might help to resolve controversies about its structural and functional organization. It has recently been proposed that the spatial orientation of Torrent-Guasp's ventricular myocardial band model (basal and apical loops) might be the mature morphological correlate of twists and torsions of the embryonic heart loop. In the present contribution, the suggestions made in this concept were analyzed in the tight of currently known facts about the development of the embryonic heart. It was found that some of the suggestions made in this concept do not correspond to embryological facts, whereas other suggestions could neither be disproved nor confirmed on the basis of our current knowledge on heart development. The answer to the question as to which of the various models of myocardial fibre organization fits best with the ontogenesis of the myocardial mass awaits future studies. The myocardial units of Torrent-Guasp's myocardial band model are said to have a functional rather than a morphological personality. Future studies on the ontogenetic development of the myocardium, therefore, should comprise not only anatomical analyses of dead specimens but should additionally comprise high resolution in vivo analyses of the development of the spatio-temporal contraction patterns of embryonic and fetal hearts. (c) 2006 Elsevier B.V. All rights reserved

    Extracardiac tissues and the epigenetic control of myocardial development in vertebrate embryos

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    During the past few years, research on the developing cardiovascular system has given new insights into the origin and development of the myocardium in vertebrate embryos. In the present paper, a review is given on our current knowledge about two aspects of myocardial development that have been found to depend on signals from extracardiac tissues. These two aspects are, firstly, the development of the so-called heart-forming fields and, secondly, the morphogenesis of the outer compact layer of the myocardial watt. (c) 2006 Elsevier GmbH. All, rights reserved

    Cardiac looping in the chick embryo: A morphological review with special reference to terminological and biomechanical aspects of the looping process

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    Understanding early cardiac morphogenesis, especially the process of cardiac looping, is of fundamental interest for diverse biomedical disciplines. During the past few years, remarkable progress has been made in identifying molecular signaling cascades involved in the control of cardiac looping. Given the rapid accumulation of new data on genetic, molecular, and cellular aspects of early cardiac morphogenesis, and given the widespread interest in cardiac looping, it seems worth reviewing those aspects of the looping process that have received less attention during the past few years. These are terminological problems, the "gross" morphological aspects, and the biomechanical concepts of cardiac looping. With respect to terminology, emphasis is given to the unperceived fact that different viewpoints exist as to which part of the normal sequence of morphogenetic events should be called cardiac looping. In a short-term version, which is preferred by developmental biologists, cardiac looping is also called dextral- or rightward-looping. Dextral-looping comprises only those morphogenetic events leading to the transformation of the originally straight heart tube into a c-shaped loop, whose convexity is normally directed toward the right of the body. Cardioembryologists, however, regard cardiac looping merely as a long-term process that may continue until the subdivisions of the heart tube and vessel primordia have approximately reached their definitive topographical relationship to each other. Among cardioembryologists, therefore, three other definitions are used. Taking into account the existence of four different definitions of the term cardiac looping will prevent some confusion in communications on early cardiac morphogenesis. With respect to the gross morphological aspects, emphasis is given to the following points. First, the straight heart tube does not consist of all future regions of the mature heart but only of the primordia of the apical trabeculated regions of the future right and left ventricles, and possibly a part of the primitive conus (outflow tract). The remaining part of the primitive conus and the primordia of the great arteries (truncus arteriosus), the inflow of both ventricles, the primitive atria, and the sinus venosus only appear during looping at the arterial (truncus arteriosus) and venous pole (other primordia). Second, dextral-looping is not simply a bending of the straight heart tube toward the right of the body, as it has frequently been misinterpreted. It results from three different morphogenetic events: (a) bending of the primitive ventricular region of the straight heart tube toward its original ventral side; (b) rotation or torsion of the bending ventricular region around a craniocaudal axis to the right of the body, so that the original ventral side of the heart tube finally forms the right convex curvature and the original dorsal side forms the left concave curvature of the c-shaped heart loop; (c) displacement of the primitive conus to the right of the body by kinking with respect to the arterial pole. Third, dextral-looping does not bring the subdivisions of the heart tube and vessel primordia approximately into their definitive topographical relationship to each other. This is achieved by the morphogenetic events following dextral-looping. This review seeks to bring together data from the diverse disciplines working on the developing heart. Anat Rec 259:248-262, 2000. (C) 2000 WiIey-Liss, Inc

    Embryology of congenital ventriculo-coronary communications: a study on quail-chick chimeras

    No full text
    Ventriculo-coronary arterial communications are rare congenital heart defects which have been explained traditionally on the basis of abnormal persistence of such communications found in the normal developing heart. Recent studies, however, have suggested that these embryonic communications might be an incidental finding rather than a normal feature. Thus, it has been suggested that congenital ventriculo-coronary communications do not represent remnants of normal embryonic vessels, but rather represent acquired lesions. In the present study, hearts were constructed in embryonic chicks in which the coronary vasculature was almost completely derived from a quail-donor. After immunohistochemical staining of the quail-derived coronary endothelium, chimeric hearts were analysed with respect to the presence of embryonic ventriculo-coronary communications, and with respect to the origin of these structures from either coronary arteries or endocardium. The results demonstrate the normal presence of ventriculo-coronary communications in avian embryonic hearts. They show, furthermore, that these structures are of coronary endothelial origin. The findings are in accord with the traditional view on the pathogenesis of congenital ventriculo-coronary communications. The roles of elevated ventricular pressure, abnormal remodelling of the developing myocardium, and of abnormal growth of the coronary vasculature are discussed relative to the pathogenesis of congenital ventriculo-coronary communications

    On rotation, torsion, lateralization, and handedness of the embryonic heart loop: New insights from a simulation model for the heart loop of chick embryos

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    The internal organs of vertebrates show specific anatomical left-right asymmetries. The embryonic heart is the first organ to develop such asymmetries during a process called dextro-looping. Thereby the initially straight heart tube curves toward its original ventral side and the resulting bend becomes displaced toward the right side of the embryo. Abnormal displacement of the heart loop toward the left is rare and is called levo-looping. Descriptive studies have shown that the lateralization of the heart loop is driven by rotation around its dorsal mesocardium. However, nothing was known on the modes of this process. To gain insight into this subject, different modes of rotation were tested in a simulation model for the looping chick embryo heart. The morphological phenotypes obtained in this model were compared with normal and mirror-imaged embryonic hearts. The following observations were made. One, rotation of the heart loop around its dorsal mesocardium has two consequences: first, lateral displacement of its bending portion either toward the right (D-loop) or left (L-loop) side of the embryo, and second, torsion of the cardiac bend into a helical structure that is wound either clockwise (right-handed helix) or counterclockwise (left-handed helix). The normal loop presents as a D-loop with left-handed helical winding and its mirror image presents as an L-loop with right-handed helical winding. This conflicts with the use to define D-loops as right- and L-loops as left-handed structures. Two, dextro-looping might be driven almost exclusively by rightward rotation of the arterial pole of the loop. It becomes complemented by leftward rotation of the venous pole during the subsequent phase of looping. An inverse mode of rotation might drive levo-looping. Three, the two different helical configurations of heart loops both can occur as right-sided, median, or left-sided positional variants. When viewed from the front, all right-sided variants appear as D-loops and all left-sided variants appear as L-loops at the end of dextro- or levo-looping. Their true asymmetric phenotypes become fully apparent only after simulation of the subsequent phase of looping. The terms D- and L-loop obviously do not fully define the chirality of heart loops. The chirality of their helical configuration should be defined, too. The implications of these data with respect to molecular and experimental data are discussed. (C) 2004 Wiley-Liss, Inc

    Does an equivalent of the "ventral node" exist in chick embryos? A scanning electron microscopic study

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    The internal organs of vertebrates show species-specific left-right (L-R) asymmetries. Questions on the embryonic origin of these asymmetries have been fascinating embryologists since the 19th century. During the past years, remarkable progress has been made in answering these questions. Evolutionary highly conserved molecular signaling cascades have been identified that start from Hensen's node and transfer side-specific identity to the embryonic left and right halves. However, the question of what initiates these signaling cascades has remained unanswered. Studies on mouse embryos have shown that: the ventral surface of Hensen's node consists of a ciliated epithelium called the ventral node. Recent findings suggest th;lt the monocilia of ventral nodel cells generate a leftward flow of extracellular fluid possibly leading to the accumulation of an unknown morphogen at the left of the node, which then might st-art the signaling cascades. This hypothesis might explain the fact that gene defects causing ciliary dyskinesia are frequently associated with situs anomalies. Studies on chick embryos led to the discovery of the L-R signaling cascades. However, whether an equivalent of the ventral node exists in avian embryos remained unknown. Therefore, I examined the endoderm and epiblast of early chick embryos for the presence of monociliated cells. In the endoderm, a population of monociliated cells indeed was present. These cells, however, were neither confined to the area of Hensen's node nor did they form the predominant cell population at this location. In the epiblast, monociliated cells formed the predominant cell population at the periphery of the blastodisc but, only a relatively small subpopulation of epiblast cells at Hensen's node. These findings suggest that, in the early chick embryo, an equivalent of the ventral node of mouse embryos neither exists on the ventral nor the dorsal surface of Hensen's node. It is unlikely that nodal cilia are required for initiating the L-R patterning in chick embryos

    A chicken model to study the embryology of cloacal exstrophy

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    Background/Purpose: The embryology of bladder and cloacal exstrophy is a mystery. Reasons for this are the lack of human embryos showing these malformations as well as the scarcity of appropriate animal models. Here, the authors present cases of cloacal exstrophies found in chick embryos subsequent to the application of suramin and trypan blue. This animal model might facilitate insight into the embryology of cloacal exstrophy. Methods: Fertilized chicken eggs were incubated at 38degreesC and 75% humidity. Embryos were treated in ovo on incubation day 3. The egg shell was windowed, and solutions of suramin (stage 13, 2 X 40 muL/0.2%) or trypan blue (stage 14, 2 X 80 muL/0.03%) were injected into the coelomic cavity. The window was closed, and the embryos were reincubated until examination on incubation day 8. Fifty embryos were treated in each group. Results: Among the surviving embryos, cloacal exstrophy was found in 2 cases in the suramin-treated group (2 of 29, 6.9%) and in 4 cases in the trypan blue-treated group (4 of 20, 20%). Conclusions: Suramin and trypan blue can induce cloacal exstrophy in chick embryos. The authors now are modifying their experimental protocols to increase the incidence of this malformation. This model might facilitate studies on the morphogenesis of cloacal exstrophy
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