DOCSLIB.ORG

Development of the Heart and Vasculature Overview

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

IN THE NAME OF GOD Development of the Heart and Vasculature Overview vascular system appears (middle of 3rd week) ◦ when the embryo is not able to satisfy its nutrition by diffusion Heart is the first functional organ ◦ beating rhythmically (22nd day) ◦ pumps blood (24-25days) single heart tube structure ◦ Myocardium ◦ Endocardium ◦ ECM (cardiac jelly) Heart development Cardiac progenitor cells in epiblast immediately lateral to primitive streak ◦ Cells migration through the cranial third of streak 1st cranial segments of heart (outflow tract) then more caudal portions right ventricle, left ventricle, and sinus venosus ◦ The cells position rostral to buccopharyngeal membrane and neural folds ◦ Splanchnic mesoderm layer ◦ They induced by underlying pharyngeal endoderm form cardiac myoblasts Blood islands also appear in this mesoderm vasculogenesis process Endothelium Blood cells ◦ horseshoe-shaped region Formation of Primitive Heart Tube Heart Tubes and Dorsal Aorta Lateral folding & Craniocaudal folding Cardiac bifida Dorsal mesocardium (Transverse pericardial sinus( • three layers Heart • Endocardium • Myocardium • Epicardium (visceral pericardium) Cardiac Looping Heart tube elongate and bend on day 23-28 cephalic portion ◦ bends ventrally, caudally, and to the right caudal portion ◦ shifts dorsal, cranial and to the left Mechanisms of cardiac bending and looping asymmetric differences in ECM composition Heart tube expansions During 5-10 weeks Atrioventricular junction sinus venosus primitive atrium ◦ L & R atrium atrioventricular junction ◦ atrioventricular canal primitive ventricle ◦ Left ventricle bulboventricular sulcus ◦ primitive interventricular foramen bulbus cordis ◦ proximal third trabeculated part of the right ventricle ◦ midportion (conus cordis) outflow tracts of both ventricles ◦ distal third (truncus arteriosus) roots and proximal portion of the aorta and pulmonary arteries aortic sac Abnormalities of Cardiac Looping Dextrocardia ◦ heart lies on right side of thorax ◦ heart loops to left instead of right ◦ may coincide with Situs inversus complete reversal of asymmetry in all organs which occurs in 1/7,000 individuals Heterotaxy ◦ 3 out of 20,000 live births ◦ sidedness is random laterality sequences predominantly left-sided bilaterally polysplenia or right-sided bilaterally asplenia or hypoplastic spleen Development of sinus venosus left horn middle of 4th week sinus venosus ◦ right and left sinus horns vitelline (omphalomesenteric) vein umbilical vein common cardinal vein Sinus entrance shifts to right ◦ left-to-right shunts of blood 4-5th week: obliteration of right umbilical vein left vitelline vein 10th week: obliteration of left common cardinal vein remnant of left sinus horn ◦ oblique vein of left atrium ◦ coronary sinus Development of sinus venosus right horn As a result of left-to-right shunts of blood right sinus horn veins enlarge greatly incorporated into the right atrium ◦ Form smooth-walled part of right atrium (sinus venarum) Development of sinus venosus sinuatrial orifice right and left venous valves ◦ dorsocranially fusion septum spurium left venous valve and septum spurium ◦ fuse with developing atrial septum right venous valve ◦ superior portion disappears entirely (crista teminalis) ◦ inferior portion develops into valve of the inferior vena cava valve of the coronary sinus Further Differentiation of the Atria Right atrium primitive right atrium ◦ trabeculated atrial ◦ pectinate muscles incorporated right sinus horn ◦ smooth-walled (sinus venarum) Left atrium primitive left atrium ◦ trabeculated atrial ◦ incorporated pulmonary veins ◦ smooth-walled part of the adult atrium Cardiac Septa Formation (Remodeling and differentiation growth) major septa formed between 27-37th days ◦ Endocardial cushions (synthesis and deposition of ECM and cell migration and proliferation) Single or Two growing cushion atrioventricular and conotruncal regions atrial septa ventricular (membranous portion) septa atrioventricular canals and valves aortic and pulmonary channels ◦ narrow tissue strip of wall fail to grow Septation of Common Atrium At the end of the 4th week Septum primum ◦ sickle-shaped crest from roof extend toward endocardial cushions of atrioventricular canal ◦ its opening: ostium primum Occlusion ostium secundum Septum secundum ◦ overlap the ostium secundum ◦ its opening: oval foramen valve of oval foramen ◦ Remnant of septum primum After birth: oval fossa ◦ lung circulation begins ◦ pressure in left atrium increases probe patency of oval foramen ◦ In about 20% of cases Atrioventricular Canal Septation At the end of 4th week Initially atrioventricular canal gives access only to the primitive left Ventricle ◦ bulbo(cono) ventricular flange to left Along base of superior endocardial cushion superior and inferior atrioventricular endocardial cushions Near the end of 5th Two lateral atrioventricular cushions Atrioventricular Valves each atrioventricular orifice surrounded by proliferations of mesenchymal tissue ◦ bloodstream hollows out and thins ventricular surface of these proliferations valves form and remain attached to ventricular wall by muscular cords papillary muscles chordae tendineae Truncus Arteriosus Septation During the fifth week pairs of truncus swellings (cushions) ◦ right superior truncus swelling grows distally and to the left ◦ left inferior truncus swelling grows distally and to the right growing swelling toward the aortic sac ◦ twist around each other After complete fusion ◦ aorticopulmonary septum Aortic channel pulmonary channel Conus Cordis Septation During the fifth week conus cordis swellings (cushions) ◦ right dorsal wall ◦ left ventral wall grow toward each other and distally unite with the truncus septum the septum divides the conus into ◦ Anterolateral (outflow of right ventricle) ◦ posteromedial (outflow of left ventricle) Ventricles Septation By the end of 4th week two primitive ventricles begin to expand by ◦ continuous growth of myocardium on outside ◦ continuous diverticulation and trabeculation on inside medial walls of expanding ventricles ◦ apposed and gradually merge muscular interventricular septum interventricular foramen ◦ outgrowth of tissue from inferior endocardial cushion ◦ membranous part of interventricular septum Semilunar Valves When partitioning of truncus is almost complete semilunar valves primordia become visible ◦ as small tubercles Then tubercles hollow out at their upper surface ◦ semilunar valves neural crest cells contribute to formation of these valves Heart Conducting System Pacemaker node ◦ Initial pacemaker caudal part of left cardiac tube cluster of cells in sinoatrial region, which derived from right common cardinal vein or right sinus venosus ◦ Later pacemaker sinus venosus ◦ Definitive pacemaker (sinuatrial node) atrioventricular node and bundle ◦ cells in left wall of sinus venosus ◦ cells from atrioventricular canal Atrial septal defect (ASD) incidence of 6.4/10,000 births ◦ premature closure of oval foramen massive hypertrophy of right atrium and ventricle underdevelopment of left side of heart Ventricular septal defect (VSD) most common congenital cardiac malformation (12/10,000 births) often associated with abnormalities in conotruncal partitioning Tetralogy of Fallot most frequently abnormality of conotruncal region (9.6/10,000 births) unequal division of conus ◦ (a) pulmonary infundibular stenosis ◦ (b) large defect of interventricular septum ◦ (c) overriding aorta arises directly above septal defect ◦ (d) hypertrophy of right ventricle Persistent truncus arteriosus conotruncal ridges fail to fuse and descend toward the ventricles (0.8/10,000 births) undivided truncus overrides both ventricles Transposition of great vessels conotruncal septum fails normal spiral course and runs straight down (4.8/10,000 births) ◦ aorta originates from right ventricle ◦ pulmonary artery originates from left ventricle sometimes is associated with a defect in membranous part of the interventricular septum usually accompanied by an open ductus arteriosus Valvular stenosis Development of the Vascular system Heart-Vasculature connections major vessels develop at same time as endocardial tube Inflow (right and left sinus horns) ◦ 3 paired vessels common cardinal veins vitelline veins umbilical veins Outflow Three pairs of aortic arch arteries and the paired dorsal aortae that circulate blood to the head and trunk 4th and 5th weeks At day 22 ◦ primitive bilateral symmetric circulatory system Vasculature Development Extraembryonic vasculature From 17th day ◦ splanchnic mesoderm of yolk sac hemangioblastic aggregates Primitive hematopoietic stem cells endothelial precursor cells By end of 3rd week blood network completely vascularizes yolk sac, connecting stalk, and chorionic villi Intraembryonic vasculature On day 18 ◦ splanchnic mesoderm of embryonic disc ◦ later in paraxial mesoderm Vasculogenesis (primary embryonic vasculature formation ) ◦ de novo blood vessel formation Endothelial precursors differentiate into endothelial cells organize into networks of small vessels Grow and invade other tissues Angiogenesis ◦ primitive vasculature expansion and remodeling ◦ Budding and sprouting from existing endothelial cords Hematopoiesis Extraembryonic hematopoiesis Primitive HSCs of yolk sac (up to 60th day) ◦ exclusively erythropoietic cells primitive erythrocytes nucleated erythrocytes containing embryonic hemoglobin
Recommended publications
  • 3 Embryology and Development

    3 Embryology and Development

    BIOL 6505 − INTRODUCTION TO FETAL MEDICINE 3. EMBRYOLOGY AND DEVELOPMENT Arlet G. Kurkchubasche, M.D. INTRODUCTION Embryology – the field of study that pertains to the developing organism/human Basic embryology –usually taught in the chronologic sequence of events. These events are the basis for understanding the congenital anomalies that we encounter in the fetus, and help explain the relationships to other organ system concerns. Below is a synopsis of some of the critical steps in embryogenesis from the anatomic rather than molecular basis. These concepts will be more intuitive and evident in conjunction with diagrams and animated sequences. This text is a synopsis of material provided in Langman’s Medical Embryology, 9th ed. First week – ovulation to fertilization to implantation Fertilization restores 1) the diploid number of chromosomes, 2) determines the chromosomal sex and 3) initiates cleavage. Cleavage of the fertilized ovum results in mitotic divisions generating blastomeres that form a 16-cell morula. The dense morula develops a central cavity and now forms the blastocyst, which restructures into 2 components. The inner cell mass forms the embryoblast and outer cell mass the trophoblast. Consequences for fetal management: Variances in cleavage, i.e. splitting of the zygote at various stages/locations - leads to monozygotic twinning with various relationships of the fetal membranes. Cleavage at later weeks will lead to conjoined twinning. Second week: the week of twos – marked by bilaminar germ disc formation. Commences with blastocyst partially embedded in endometrial stroma Trophoblast forms – 1) cytotrophoblast – mitotic cells that coalesce to form 2) syncytiotrophoblast – erodes into maternal tissues, forms lacunae which are critical to development of the uteroplacental circulation.
  • Te2, Part Iii

    Te2, Part Iii

    TERMINOLOGIA EMBRYOLOGICA Second Edition International Embryological Terminology FIPAT The Federative International Programme for Anatomical Terminology A programme of the International Federation of Associations of Anatomists (IFAA) TE2, PART III Contents Caput V: Organogenesis Chapter 5: Organogenesis (continued) Systema respiratorium Respiratory system Systema urinarium Urinary system Systemata genitalia Genital systems Coeloma Coelom Glandulae endocrinae Endocrine glands Systema cardiovasculare Cardiovascular system Systema lymphoideum Lymphoid system Bibliographic Reference Citation: FIPAT. Terminologia Embryologica. 2nd ed. FIPAT.library.dal.ca. Federative International Programme for Anatomical Terminology, February 2017 Published pending approval by the General Assembly at the next Congress of IFAA (2019) Creative Commons License: The publication of Terminologia Embryologica is under a Creative Commons Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0) license The individual terms in this terminology are within the public domain. Statements about terms being part of this international standard terminology should use the above bibliographic reference to cite this terminology. The unaltered PDF files of this terminology may be freely copied and distributed by users. IFAA member societies are authorized to publish translations of this terminology. Authors of other works that might be considered derivative should write to the Chair of FIPAT for permission to publish a derivative work. Caput V: ORGANOGENESIS Chapter 5: ORGANOGENESIS
  • Abnormal Embryonic Lymphatic Vessel Development in Tie1 Hypomorphic Mice Xianghu Qu, Kevin Tompkins, Lorene E

    Abnormal Embryonic Lymphatic Vessel Development in Tie1 Hypomorphic Mice Xianghu Qu, Kevin Tompkins, Lorene E

    © 2014. Published by The Company of Biologists Ltd | Development (2014) 141, 1417 doi:10.1242/dev.108969 CORRECTION Abnormal embryonic lymphatic vessel development in Tie1 hypomorphic mice Xianghu Qu, Kevin Tompkins, Lorene E. Batts, Mira Puri and H. Scott Baldwin There was an error published in Development 137, 1285-1295. Author name H. Scott Baldwin was incomplete. The correct author list appears above. The authors apologise to readers for this mistake. 1417 RESEARCH ARTICLE 1285 Development 137, 1285-1295 (2010) doi:10.1242/dev.043380 © 2010. Published by The Company of Biologists Ltd Abnormal embryonic lymphatic vessel development in Tie1 hypomorphic mice Xianghu Qu1, Kevin Tompkins1, Lorene E. Batts1, Mira Puri2 and Scott Baldwin1,3,* SUMMARY Tie1 is an endothelial receptor tyrosine kinase that is essential for development and maintenance of the vascular system; however, the role of Tie1 in development of the lymphatic vasculature is unknown. To address this question, we first documented that Tie1 is expressed at the earliest stages of lymphangiogenesis in Prox1-positive venous lymphatic endothelial cell (LEC) progenitors. LEC Tie1 expression is maintained throughout embryonic development and persists in postnatal mice. We then generated two lines of Tie1 mutant mice: a hypomorphic allele, which has reduced expression of Tie1, and a conditional allele. Reduction of Tie1 levels resulted in abnormal lymphatic patterning and in dilated and disorganized lymphatic vessels in all tissues examined and in impaired lymphatic drainage in embryonic skin. Homozygous hypomorphic mice also exhibited abnormally dilated jugular lymphatic vessels due to increased production of Prox1-positive LECs during initial lymphangiogenesis, indicating that Tie1 is required for the early stages of normal lymphangiogenesis.
  • CCM2 and CCM3 Proteins Contribute to Vasculogenesis and Angiogenesis in Human Placenta

    CCM2 and CCM3 Proteins Contribute to Vasculogenesis and Angiogenesis in Human Placenta

    Histol Histopathol (2009) 24: 1287-1294 Histology and http://www.hh.um.es Histopathology Cellular and Molecular Biology CCM2 and CCM3 proteins contribute to vasculogenesis and angiogenesis in human placenta Gamze Tanriover1, Yasemin Seval1, Leyla Sati1, Murat Gunel2 and Necdet Demir1 1Department of Histology and Embryology, Akdeniz University, School of Medicine, Antalya, Turkey and 2 Department of Neurosurgery, Yale University, School of Medicine, New Haven, CT, USA Summary. Placenta as an ideal model to study Introduction angiogenic mechanisms have been established in previous studies. There are two processes, The placenta is a multifaceted organ that plays a vasculogenesis and angiogenesis, involved in blood critical role in maintaining and protecting the developing vessel formation during placental development. fetus. Normal development and function of the placenta Therefore, blood vessel formation is a crucial issue that requires extensive vasculogenesis and subsequent might cause vascular malformations. One of the vascular angiogenesis, in both maternal and fetal tissues. malformations is cerebral cavernous malformation Vasculogenesis is the formation of the primitive vascular (CCM) in the central nervous system, consisting of network de novo from progenitor cells, and angiogenesis endothelium-lined vascular channels without intervening is identified as the extension of blood vessels from normal brain parenchyma. Three CCM loci have been preexisting vascular structures (Demir et al., 1989, 2006; mapped as Ccm1, Ccm2, Ccm3 genes in CCM. In order Geva et al., 2002; Charnock-Jones et al., 2004). Many to investigate whether CCM proteins participate in blood factors, such as vascular endothelial growth factor vessel formation, we report here the expression patterns (VEGF), angiopoietins (Angpt-1 and -2) and their of CCM2 and CCM3 in developing and term human receptors are involved in the molecular regulation of placenta by means of immunohistochemistry and these diverse developmental steps.
  • Download PDF Version

    Download PDF Version

    FIG. 4–1 Dorsal aspect of the 10-somite embryo. 24 IV the fourth week of life somite and neural tube period I. EMBRYO PROPER caudal openings of the tube are called neuropores. The rostral neuropore closes between 18 and 20 somites. The caudal neuro- A. EXTERNAL APPEARANCE pore closes at 25 somites. Figs. 4–1, 4–2 1. The specimens measure approximately 1 to 3.5 mm in length Brain and have 1 to 29 pairs of somites. Three brain subdivisions are present in the cranial portion of the 2. The head and tail folds move the attachment of the amnion tube and are named, from cranial to caudal, the prosencephalon, to the ventral side of the head and tail regions, respectively. mesencephalon and rhombencephalon. The boundary between the The lateral body folds move the amnion attachment to the pros- and mesencephalon is demarcated by a ventral bend, called ventrolateral surface in the midportion of the embryo. the cephalic flexure. An external groove and a prominent swelling 3. The head region is elevated above the yolk sac by the large on the medial surface of the neural plate may also demarcate the pericardial sac, the midportion lies upon the yolk sac and the boundary. The boundary between the mes- and rhombencephalon caudal region is curved toward the yolk sac. is distinguished by a groove on the medial and lateral surfaces of 4. The embryo possesses somites, which are apparent through the neural plate or tube. the ectoderm. 5. The neural tube develops from the neural plate and remains Prosencephalon open at each end for 2 to 4 days.
  • Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All V Integrins

    Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All V Integrins

    Cell, Vol. 95, 507–519, November 13, 1998, Copyright ©1998 by Cell Press Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All ␣v Integrins Bernhard L. Bader,*‡ Helen Rayburn,* their ligands. Significant expression of ␣v integrins has Denise Crowley,* and Richard O. Hynes*† been noted, in particular, in neural crest cells (Delannet * Howard Hughes Medical Institute et al., 1994), glial cells (Hirsch et al., 1994; Milner and Center for Cancer Research ffrench-Constant, 1994), muscle (Hirsch et al., 1994; Mc- and Department of Biology Donald et al., 1995; Martin and Sanes, 1997), osteoclasts Massachusetts Institute of Technology (Va¨ a¨ na¨ nen and Horton, 1995), epithelia (␣v␤6; Breuss et Cambridge, Massachusetts 02139 al., 1995; Huang et al., 1996), and blood vessels during development (Brooks et al., 1994a; Drake et al., 1995; Friedlander et al., 1995, 1996) or angiogenesis in re- Summary sponse to tumors (Brooks et al., 1994a, 1994b, 1996, 1998; Varner et al., 1995). ␣v integrins have been implicated in many develop- Among the ligands for various ␣v␤ integrins is fibro- mental processes and are therapeutic targets for inhi- nectin (FN), and results on mouse embryos lacking FN bition of angiogenesis and osteoporosis. Surprisingly, or FN receptor integrins suggest that ␣v integrins might ablation of the gene for the ␣v integrin subunit, elimi- be important receptors for FN during early development. nating all five ␣v integrins, although causing lethality, FN-null embryos fail to form notochord or somites allows considerable development and organogenesis (George et al., 1993; Georges-Labouesse et al., 1996), including, most notably, extensive vasculogenesis and whereas embryos null for either (Yang et al., 1993, 1995) angiogenesis.
  • Copyright by Steven A. Vokes 2002 the Dissertation Committee for Steven Alexander Vokes Certifies That This Is the Approved Version of the Following Dissertation

    Copyright by Steven A. Vokes 2002 the Dissertation Committee for Steven Alexander Vokes Certifies That This Is the Approved Version of the Following Dissertation

    Copyright by Steven A. Vokes 2002 The Dissertation Committee for Steven Alexander Vokes Certifies that this is the approved version of the following dissertation: The Role of Endoderm in Vascular Patterning Committee: Janice A. Fischer, Supervisor Paul A. Krieg , Co-Supervisor Alan M. Lloyd Arlen W. Johnson S. Martin Shankland R. Adron Harris The Role of Endoderm in Vascular Patterning by Steven Alexander Vokes, B.A. Dissertation Presented to the Faculty of the Graduate School of The University of Texas at Austin in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy The University of Texas at Austin December, 2002 Dedication This work, symbolic of my higher education, is dedicated to my parents Carol and Emmett Vokes, who played such an integral role in its foundations. Acknowledgements I have been extremely fortunate to have excellent mentoring during my time in graduate school. I thank Paul Krieg for his suggestions, enthusiasm, encouragement and friendship during this learning process. He has taught me how to think (and write) critically and insightfully about science. I am also grateful to Amy Cheng Vollmer, my undergraduate mentor. She introduced me to the joys of scientific research, and continues to give me excellent advice whenever I need it most. I thank Peter Vize, whose conversations led to the first experiments described within. In daily interactions, I have benefited from a caste of talented co-workers and advisors. These include Craig Newman, Wendy Gerber, Ondine Cleaver, Tom Carroll, Eric Small, Rob Garriock, Martha Joe, Parker Antin, Ray Runyan, Jean Wilson, Carol Gregorio and all past and present members of the Krieg lab.
  • The Evolving Cardiac Lymphatic Vasculature in Development, Repair and Regeneration

    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.
  • Glossary of Key Terms and Concepts - Chapter 8

    Glossary of Key Terms and Concepts - Chapter 8

    Glossary of Key Terms and Concepts - Chapter 8 Angioblasts - These "vessel-forming cells" may arise from any kind of mesoderm except prechordal plate mesoderm. Angioblastic cords - Angiocysts coalesce to form short blind-ended angioblastic cords. Angioblastic plexuses - Angioblastic cords coalesce to form complex interconnected vascular networks or plexuses. Angiocysts - These vesicles are formed by angioblasts during the process of vasculogenesis. Angiogenesis - This is the mechanism whereby preexisting vessels lengthen or branch by sprouting. Aortic arches - These vessels have been modified in humans to form the great vessels of the thorax (also see Ch. 7). Axis arteries - These central arteries of the limbs are derived from the 7th intersegmental arteries (upper limb) and 5th lumbar intersegmental arteries (lower limb). Blood islands - Blood islands are cysts of angioblasts containing hemoblasts. These coalesce to form blood vessels in the yolk sac and also form the coronary vasculature. Branchial arches - These are the gill bars of fish. Homologous structures of humans are more appropriately named "pharyngeal" arches. Cardinal system of veins - These veins drain the head and neck and body wall and extremities of the embryo. Anterior cardinals drain the head and neck and the trunk and lower extremities are drained by paired posterior cardinals. The posterior cardinal veins are replaced by subcardinal and supracardinal veins during the second month. Coronary vessels - These vessels of the heart form from epicardium as subepicardial plexuses fuse with sprouts of the aorta and coronary sinus to form the coronary arteries and coronary veins respectively. Endothelial cells - These cells arise from angioblasts to form the initial vascular network.
  • Development of HEART 4-VEINS

    Development of HEART 4-VEINS

    Development of brachiocephalic veins 1. Right brachiocephalic vein is formed by cranial part of right anterior cardinal vein and 2. Left brachiocephalic is formed by cranial part of left anterior cardinal vein and the interant.cardinal anastomosis. Development of superior vena cava 1. The part up to the opening of vena azygos develops from caudal part of right ant.cardinal vein and 2. The part below the opening (intrapericardial part) is formed by the right common cardinal vein. Development of azygos and hemiazygos veins A. 1. Vena azygos develops from right azygos line vein and 2. The arch of vena azygos is formed by the cranial end of right postcardinal vein. B. Hemiazygos veins are formed by the left azygos line vein. Development of Inferior vena cava Inferior vena cava is formed, from below upwards by: 1. Begins by the union of the two common iliac veins (postcardinal veins), 2. Right supracardinal, 3. Right supra-subcardinal anastomosis, 4. Right subcardinal, 5. New formation (hepatic segment) and 6. Hepatocardiac channel (terminal part of right vitelline vein). Congenital anomalies • Double inferior vena cava • Absence • Left SVC • Double SVC DEVELOPMENT OF PORTAL VEIN 1. The portal vein is formed behind the neck of pancreas by the union of superior mesentric and splenic vein to the left vitelline vein. 2. The part of the portal vein which is behind the Ist part of duodenum is formed by middle dorsal transverse anastomosis. 3. Part of portal vein which is in the free margin of lesser omentum is formed by cranial or distal part of right vitelline vein.
  • Azygos Vein System Abnormality: Case Report

    Azygos Vein System Abnormality: Case Report

    Gülhane Týp Dergisi 2006; 48: 180-182 OLGU SUNUMU © Gülhane Askeri Týp Akademisi 2006 Azygos vein system abnormality: case report Necdet Kocabýyýk (*), Tunç Kutoðlu (**), Soner Albay (*), Bülent Yalçýn (*), Hasan Ozan (*) Summary Introduction Variations seen in the thoracic vein system are Abnormalities related to the azygos system are not rare (1). In a series related to the development of these veins. of 200 cases, Bergman et al. have reported the incidence of this anomaly During the dissection from the posterior medi- astinum of the 60-year-old male cadaver, it 26% (2). These abnormalities are generally explained by the embryolog- was observed that there was no complete ical development. Venous branching of the azygos vein varies (3). There accessory hemiazygos vein, and both posterior are two origins of the azygos and hemiazygos veins. By union of these intercostal veins and hemiazygos vein (above origins and regression of some parts, azygos system comes into its final T10 level) drained bilaterally to the azygos vein. Considering these types of variations is status (4). Different types of structures may occur when these veins important during imaging this region and surgi- develop. Abnormalities about azygos system and especially the variations cal operations. of the hemiazygos veins are not clearly described in the literature. In this Key words: Azygos vein, hemiazygos vein, superior vena cava, venous anomaly presentation absence of the accessory hemiazygos vein and possible causes of these types of variations are discussed in view of the embry- Özet ological development. Azigos ven sistem anomalisi: olgu sunumu Toraks ven sisteminde görülen varyasyonlar, embriyolojik olarak bu venlerin geliþimiyle ilgi- Case Report lidir.
  • Cardiovascular System Heart Development Cardiovascular System Heart Development

    Cardiovascular System Heart Development Cardiovascular System Heart Development

    Cardiovascular System Heart Development Cardiovascular System Heart Development In human embryos, the heart begins to beat at approximately 22-23 days, with blood flow beginning in the 4th week. The heart is one of the earliest differentiating and functioning organs. • This emphasizes the critical nature of the heart in distributing blood through the vessels and the vital exchange of nutrients, oxygen, and wastes between the developing baby and the mother. • Therefore, the first system that completes its development in the embryo is called cardiovascular system. https://www.slideshare.net/DrSherifFahmy/intraembryonic-mesoderm-general-embryology Mesoderm is one of the three • Connective tissue primary germ layers that • Smooth and striated muscle • Cardiovascular System differentiates early in • Kidneys development that collectively • Spleen • Genital organs, ducts gives rise to all subsequent • Adrenal gland cortex tissues and organs. The cardiovascular system begins to develop in the third week of gestation. Blood islands develop in the newly formed mesoderm, and consist of (a) a central group of haemoblasts, the embryonic precursors of blood cells; (b) endothelial cells. Development of the heart and vascular system is often described together as the cardiovascular system. Development begins very early in mesoderm both within (embryonic) and outside (extra embryonic, vitelline, umblical and placental) the embryo. Vascular development occurs in many places. • Blood islands coalesce to form a vascular plexus. Preferential channels form arteries and veins. • Day 17 - Blood islands form first in the extra-embryonic mesoderm • Day 18 - Blood islands form next in the intra-embryonic mesoderm • Day 19 - Blood islands form in the cardiogenic mesoderm and coalesce to form a pair of endothelial heart tubes Development of a circulation • A circulation is established during the 4th week after the myocardium is differentiated.