The Heart a Very Effective Pump, Moves Blood Through the CS and Also by Aspiration
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Coronary Arterial Development Is Regulated by a Dll4-Jag1-Ephrinb2 Signaling Cascade
RESEARCH ARTICLE Coronary arterial development is regulated by a Dll4-Jag1-EphrinB2 signaling cascade Stanislao Igor Travisano1,2, Vera Lucia Oliveira1,2, Bele´ n Prados1,2, Joaquim Grego-Bessa1,2, Rebeca Pin˜ eiro-Sabarı´s1,2, Vanesa Bou1,2, Manuel J Go´ mez3, Fa´ tima Sa´ nchez-Cabo3, Donal MacGrogan1,2*, Jose´ Luis de la Pompa1,2* 1Intercellular Signalling in Cardiovascular Development and Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; 2CIBER de Enfermedades Cardiovasculares, Madrid, Spain; 3Bioinformatics Unit, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain Abstract Coronaries are essential for myocardial growth and heart function. Notch is crucial for mouse embryonic angiogenesis, but its role in coronary development remains uncertain. We show Jag1, Dll4 and activated Notch1 receptor expression in sinus venosus (SV) endocardium. Endocardial Jag1 removal blocks SV capillary sprouting, while Dll4 inactivation stimulates excessive capillary growth, suggesting that ligand antagonism regulates coronary primary plexus formation. Later endothelial ligand removal, or forced expression of Dll4 or the glycosyltransferase Mfng, blocks coronary plexus remodeling, arterial differentiation, and perivascular cell maturation. Endocardial deletion of Efnb2 phenocopies the coronary arterial defects of Notch mutants. Angiogenic rescue experiments in ventricular explants, or in primary human endothelial cells, indicate that EphrinB2 is a critical effector of antagonistic Dll4 and Jag1 functions in arterial morphogenesis. Thus, coronary arterial precursors are specified in the SV prior to primary coronary plexus formation and subsequent arterial differentiation depends on a Dll4-Jag1-EphrinB2 signaling *For correspondence: [email protected] (DMG); cascade. [email protected] (JLP) Competing interests: The authors declare that no Introduction competing interests exist. -
The Ventricles
Guest Editorial Evolution of the Ventricles Solomon Victor, FRCS, FRCP We studied the evolution of ventricles by macroscopic examination of the hearts of Vijaya M. Nayak, MS marine cartilaginous and bony fish, and by angiocardiography and gross examination of Raveen Rajasingh, MPhil the hearts of air-breathing freshwater fish, frogs, turtles, snakes, and crocodiles. A right-sided, thin-walled ventricular lumen is seen in the fish, frog, turtle, and snake. In fish, there is external symmetry of the ventricle, internal asymmetry, and a thick- walled left ventricle with a small inlet chamber. In animals such as frogs, turtles, and snakes, the left ventricle exists as a small-cavitied contractile sponge. The high pressure generated by this spongy left ventricle, the direction of the jet, the ventriculoarterial ori- entation, and the bulbar spiral valve in the frog help to separate the systemic and pul- monary circulations. In the crocodile, the right aorta is connected to the left ventricle, and there is a complete interventricular septum and an improved left ventricular lumen when compared with turtles and snakes. The heart is housed in a rigid pericardial cavity in the shark, possibly to protect it from changing underwater pressure. The pericardial cavity in various species permits move- ments of the heart-which vary depending on the ventriculoarterial orientation and need for the ventricle to generate torque or spin on the ejected blood- that favor run-off into the appropriate arteries and their branches. In the lower species, it is not clear whether the spongy myocardium contributes to myocardial oxygenation. In human beings, spongy myocardium constitutes a rare form of congenital heart disease. -
Fetal Blood Flow and Genetic Mutations in Conotruncal Congenital Heart Disease
Journal of Cardiovascular Development and Disease Review Fetal Blood Flow and Genetic Mutations in Conotruncal Congenital Heart Disease Laura A. Dyer 1 and Sandra Rugonyi 2,* 1 Department of Biology, University of Portland, Portland, OR 97203, USA; [email protected] 2 Department of Biomedical Engineering, Oregon Health & Science University, Portland, OR 97239, USA * Correspondence: [email protected] Abstract: In congenital heart disease, the presence of structural defects affects blood flow in the heart and circulation. However, because the fetal circulation bypasses the lungs, fetuses with cyanotic heart defects can survive in utero but need prompt intervention to survive after birth. Tetralogy of Fallot and persistent truncus arteriosus are two of the most significant conotruncal heart defects. In both defects, blood access to the lungs is restricted or non-existent, and babies with these critical conditions need intervention right after birth. While there are known genetic mutations that lead to these critical heart defects, early perturbations in blood flow can independently lead to critical heart defects. In this paper, we start by comparing the fetal circulation with the neonatal and adult circulation, and reviewing how altered fetal blood flow can be used as a diagnostic tool to plan interventions. We then look at known factors that lead to tetralogy of Fallot and persistent truncus arteriosus: namely early perturbations in blood flow and mutations within VEGF-related pathways. The interplay between physical and genetic factors means that any one alteration can cause significant disruptions during development and underscore our need to better understand the effects of both blood flow and flow-responsive genes. -
The Evolving Cardiac Lymphatic Vasculature in Development, Repair and Regeneration
REVIEWS The evolving cardiac lymphatic vasculature in development, repair and regeneration Konstantinos Klaourakis 1,2, Joaquim M. Vieira 1,2,3 ✉ and Paul R. Riley 1,2,3 ✉ Abstract | The lymphatic vasculature has an essential role in maintaining normal fluid balance in tissues and modulating the inflammatory response to injury or pathogens. Disruption of normal development or function of lymphatic vessels can have severe consequences. In the heart, reduced lymphatic function can lead to myocardial oedema and persistent inflammation. Macrophages, which are phagocytic cells of the innate immune system, contribute to cardiac development and to fibrotic repair and regeneration of cardiac tissue after myocardial infarction. In this Review, we discuss the cardiac lymphatic vasculature with a focus on developments over the past 5 years arising from the study of mammalian and zebrafish model organisms. In addition, we examine the interplay between the cardiac lymphatics and macrophages during fibrotic repair and regeneration after myocardial infarction. Finally, we discuss the therapeutic potential of targeting the cardiac lymphatic network to regulate immune cell content and alleviate inflammation in patients with ischaemic heart disease. The circulatory system of vertebrates is composed of two after MI. In this Review, we summarize the current complementary vasculatures, the blood and lymphatic knowledge on the development, structure and function vascular systems1. The blood vasculature is a closed sys- of the cardiac lymphatic vasculature, with an emphasis tem responsible for transporting gases, fluids, nutrients, on breakthroughs over the past 5 years in the study of metabolites and cells to the tissues2. This extravasation of cardiac lymphatic heterogeneity in mice and zebrafish. -
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Folia Morphol. Vol. 78, No. 2, pp. 283–289 DOI: 10.5603/FM.a2018.0077 O R I G I N A L A R T I C L E Copyright © 2019 Via Medica ISSN 0015–5659 journals.viamedica.pl Observations of foetal heart veins draining directly into the left and right atria J.H. Kim1, O.H. Chai1, C.H. Song1, Z.W. Jin2, G. Murakami3, H. Abe4 1Department of Anatomy and Institute of Medical Sciences, Chonbuk National University Medical School, Jeonju, Korea 2Department of Anatomy, Wuxi Medical School, Jiangnan University, Wuxi, China 3Division of Internal Medicine, Jikou-kai Clinic of Home Visits, Sapporo, Japan 4Department of Anatomy, Akita University School of Medicine, Akita, Japan [Received: 19 June 2018; Accepted: 8 August 2018] Evaluation of semiserial sections of 14 normal hearts from human foetuses of gestational age 25–33 weeks showed that all of these hearts contained thin veins draining directly into the atria (maximum, 10 veins per heart). Of the 75 veins in these 14 hearts, 55 emptied into the right atrium and 20 into the left atrium. These veins were not accompanied by nerves, in contrast to tributaries of the great cardiac vein, and were negative for both smooth muscle actin (SMA) and CD34. However, the epithelium and venous wall of the anterior cardiac vein, the thickest of the direct draining veins, were strongly positive for SMA and CD34, respectively. In general, developing fibres in the vascular wall were positive for CD34, while the endothelium of the arteries and veins was strongly positive for the present DAKO antibody of SMA. -
Location of the Human Sinus Node in Black Africans
ogy: iol Cu ys r h re P n t & R y e s Anatomy & Physiology: Current m e o a t r a c n h A Research Meneas et al., Anat Physiol 2017, 7:5 ISSN: 2161-0940 DOI: 10.4172/2161-0940.1000279 Research article Open Access Location of the Human Sinus Node in Black Africans Meneas GC*, Yangni-Angate KH, Abro S and Adoubi KA Department of Cardiovascular and Thoracic Diseases, Bouake Teaching Hospital, Cote d’Ivoire, West-Africa *Corresponding author: Meneas GC, Department of Cardiovascular and Thoracic Diseases, Bouake Teaching Hospital, Cote d’Ivoire, West-Africa, Tel: +22507701532; E-mail: [email protected] Received Date: August 15, 2017; Accepted Date: August 22, 2017; Published Date: August 29, 2017 Copyright: © 2017 Meneas GC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited. Abstract Objective: The purpose of this study was to describe, in 45 normal hearts of black Africans adults, the location of the sinoatrial node. Methods: After naked eye observation of the external epicardial area of the sinus node classically described as cavoatrial junction (CAJ), a histological study of the sinus node area was performed. Results: This study concluded that the sinus node is indistinguishable to the naked eye (97.77% of cases), but still identified histologically at the CAJ in the form of a cluster of nodal cells surrounded by abundant connective tissues. It is distinguished from the Myocardial Tissue. -
4B. the Heart (Cor) 1
Henry Gray (1821–1865). Anatomy of the Human Body. 1918. 4b. The Heart (Cor) 1 The heart is a hollow muscular organ of a somewhat conical form; it lies between the lungs in the middle mediastinum and is enclosed in the pericardium (Fig. 490). It is placed obliquely in the chest behind the body of the sternum and adjoining parts of the rib cartilages, and projects farther into the left than into the right half of the thoracic cavity, so that about one-third of it is situated on the right and two-thirds on the left of the median plane. Size.—The heart, in the adult, measures about 12 cm. in length, 8 to 9 cm. in breadth at the 2 broadest part, and 6 cm. in thickness. Its weight, in the male, varies from 280 to 340 grams; in the female, from 230 to 280 grams. The heart continues to increase in weight and size up to an advanced period of life; this increase is more marked in men than in women. Component Parts.—As has already been stated (page 497), the heart is subdivided by 3 septa into right and left halves, and a constriction subdivides each half of the organ into two cavities, the upper cavity being called the atrium, the lower the ventricle. The heart therefore consists of four chambers, viz., right and left atria, and right and left ventricles. The division of the heart into four cavities is indicated on its surface by grooves. The atria 4 are separated from the ventricles by the coronary sulcus (auriculoventricular groove); this contains the trunks of the nutrient vessels of the heart, and is deficient in front, where it is crossed by the root of the pulmonary artery. -
Cardiogenesis with a Focus on Vasculogenesis and Angiogenesis
Received: 27 August 2019 | Revised: 4 February 2020 | Accepted: 20 February 2020 DOI: 10.1111/ahe.12549 SPECIAL ISSUE Cardiogenesis with a focus on vasculogenesis and angiogenesis Katrin Borasch1 | Kenneth Richardson2 | Johanna Plendl1 1Department of Veterinary Medicine, Institute of Veterinary Anatomy, Freie Abstract University Berlin, Berlin, Germany The initial intraembryonic vasculogenesis occurs in the cardiogenic mesoderm. Here, 2 College of Veterinary Medicine, School a cell population of proendocardial cells detaches from the mesoderm that subse- of Veterinary and Life Sciences, Murdoch University, Murdoch, WA, Australia quently generates the single endocardial tube by forming vascular plexuses. In the course of embryogenesis, the endocardium retains vasculogenic, angiogenic and Correspondence Johanna Plendl, Department of Veterinary haematopoietic potential. The coronary blood vessels that sustain the rapidly ex- Medicine, Institute of Veterinary Anatomy, panding myocardium develop in the course of the formation of the cardiac loop by Freie University Berlin, Berlin, Germany. Email: [email protected] vasculogenesis and angiogenesis from progenitor cells of the proepicardial serosa at the venous pole of the heart as well as from the endocardium and endothelial cells of Funding information Freie Universität Berlin the sinus venosus. Prospective coronary endothelial cells and progenitor cells of the coronary blood vessel walls (smooth muscle cells, perivascular cells) originate from different cell populations that are in close spatial as well as regulatory connection with each other. Vasculo- and angiogenesis of the coronary blood vessels are for a large part regulated by the epicardium and epicardium-derived cells. Vasculogenic and angiogenic signalling pathways include the vascular endothelial growth factors, the angiopoietins and the fibroblast growth factors and their receptors. -
Sudden Death in Racehorses: Postmortem Examination Protocol
VDIXXX10.1177/1040638716687004Sudden death in racehorsesDiab et al. 687004research-article2017 Special Issue Journal of Veterinary Diagnostic Investigation 1 –8 Sudden death in racehorses: postmortem © 2017 The Author(s) Reprints and permissions: sagepub.com/journalsPermissions.nav examination protocol DOI: 10.1177/1040638716687004 jvdi.sagepub.com Santiago S. Diab,1 Robert Poppenga, Francisco A. Uzal Abstract. In racehorses, sudden death (SD) associated with exercise poses a serious risk to jockeys and adversely affects racehorse welfare and the public perception of horse racing. In a majority of cases of exercise-associated sudden death (EASD), there are no gross lesions to explain the cause of death, and an examination of the cardiovascular system and a toxicologic screen are warranted. Cases of EASD without gross lesions are often presumed to be sudden cardiac deaths (SCD). We describe an equine SD autopsy protocol, with emphasis on histologic examination of the heart (“cardiac histology protocol”) and a description of the toxicologic screen performed in racehorses in California. By consistently utilizing this standardized autopsy and cardiac histology protocol, the results and conclusions from postmortem examinations will be easier to compare within and across institutions over time. The generation of consistent, reliable, and comparable multi-institutional data is essential to improving the understanding of the cause(s) and pathogenesis of equine SD, including EASD and SCD. Key words: Cardiac autopsy; equine; exercise; racehorses; -
Endocardial Cushion and Myocardial Defects After Cardiac Myocyte-Specific Conditional Deletion of the Bone Morphogenetic Protein Receptor ALK3
Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3 Vinciane Gaussin*†, Tom Van de Putte‡, Yuji Mishina§, Mark C. Hanks¶, An Zwijsen‡, Danny Huylebroeck‡, Richard R. Behringerʈ, and Michael D. Schneider*,** *Center for Cardiovascular Development, Baylor College of Medicine, Houston, TX 77030; ‡Flanders Interuniversity Institute for Biotechnology (VIB07), K.U. Leuven, 3000 Leuven, Belgium; §National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709; ¶Procter and Gamble Pharmaceuticals Health Care Research Center, 8700 Mason Montgomery Road, Mason, OH 45040; and ʈUniversity of Texas–M. D. Anderson Cancer Center, Houston, TX 77030 Edited by Eric N. Olson, University of Texas Southwestern Medical Center, Dallas, TX, and approved December 31, 2001 (received for review July 26, 2001) Receptors for bone morphogenetic proteins (BMPs), members of velopment, whereas ALK6 is absent from the heart at mid- the transforming growth factor- (TGF) superfamily, are persis- gestation (17). The developing heart also expresses ALK2͞ tently expressed during cardiac development, yet mice lacking type ActRIA (5, 18), which can function as a type I BMP receptor II or type IA BMP receptors die at gastrulation and cannot be used with preference for BMP6 and -7 (19). ALK3, ALK2, and to assess potential later roles in creation of the heart. Here, we BMPR-II are each essential for gastrulation and mesoderm used a Cre͞lox system for cardiac myocyte-specific deletion of the formation (18, 20, 21); mice lacking just BMP4 also fail to type IA BMP receptor, ALK3. ALK3 was specifically required at progress, typically, beyond the egg cylinder stage (22). -
Ventricular Septal Defect (VSD)
Ventricular Septal Defect (VSD) Ventricular Septal Defect. Flow of blood through a normal heart. What is a Ventricular Septal Defect?Your pet has been diagnosed with a Ventricular Septal Defect (VSD). A VSD is a malformation of the wall (interventricular septum) between the two pumping chambers (ventricles) allowing an abnormal communication. A VSD is a type of congenital defect, which means it is present from birth. VSDs are classified based upon whether they are restrictive or non-restrictive. In order to understand how this disease may affect your dog, it is important to understand normal circulation in the heart. Blood drains from the body into the right collecting chamber (called “atrium”) where it passes through the tricuspid valve and into the right pumping chamber (called “ventricle”). From here, blood is pumped into the pulmonary artery and subsequently to the lungs where it picks up oxygen. The oxygenated blood then drains passively into the left atrium, through the mitral valve, and into the left ventricle. The left ventricle then pumps the blood through the aorta and back to the body. Restrictive VSD: A restrictive VSD is a smaller diameter VSD that provides resistance of blood flow. These are the most common VSDs that we diagnose in dogs and cats. Due to normally higher pressures in the left side of the heart compared to the right side of the heart, most have blood flow from left-to-right through the hole. The amount of blood shunted depends on size of the VSD and the pressure difference across the VSD. Therefore, restrictive VSDs are further classified based on whether they are “hemodynamically significant” or not. -
Ultrastructure of the Normal Atrial Endocardium R
Brit. Heart J., 1966, 28, 785. Ultrastructure of the Normal Atrial Endocardium R. A. LANNIGAN AND SALEH A. ZAKI From the Department of Pathology, University of Birmingham, and the Department of Pathology, University of Assiut, U.A.R. Surgical biopsies of the heart and early needle Thin sections were then cut and examined on an A.E.I. "biopsies" at necropsy now permit ultrastructural E M 6 electron microscope. investigations into many cardiac conditions. There For light microscopy, blocks of the whole circum- are, however, very few such studies on normal human ference were embedded in paraffin and sections were stained with Ehrlich's hTmatoxylin and eosin, van myocardium and none are available on human or Gieson's stain, Lawson's modification of the Weigert- animal endocardium. The commonest surgical Sheridan elastic stain, the periodic-acid Schiff reaction, specimens from the heart are from the left or right and Hale's dialysed iron. atrial appendages, and this material has been used to study normal structure, as a baseline for the investigation of cardiac diseases such as rheumatic RESULTS heart disease and fibro-elastosis, etc. For obvious Light Microscopy reasons, it is difficult to obtain fresh material from "normal" hearts, and specimens were selected for The structure of the left atrial wall has been electron microscopy which were within normal described by Koniger (1903), Nagayo (1909), Von limits on the light microscope (Lannigan, 1959). Glahn (1926), and Gross (1935), and the structure of the atrial appendages, which was shown to be similar to that of the atrium, was described by MATERIAL AND METHODS Waaler (1952), Lannigan (1959), and Ling, Wang, Three left atrial appendages and three right append- and Kuo (1959).