DOCSLIB.ORG

Embryonic Vascular Development: Immunohistochemical Identification of the Origin and Subsequent Morphogenesis of the Major Vessel Primordia in Quail Embryos

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Embryonic Vascular Development: Immunohistochemical Identification of the Origin and Subsequent Morphogenesis of the Major Vessel Primordia in Quail Embryos Development 102, 735-748 (1988) 735 Printed in Great Britain © The Company of Biologists Limited 1988 Embryonic vascular development: immunohistochemical identification of the origin and subsequent morphogenesis of the major vessel primordia in quail embryos J. DOUGLAS COFFIN and THOMAS J. POOLE Department of Anatomy and Cell Biology, SUNY Health Science Center at Syracuse, 766 Irving Avenue, Syracuse, NY 13210, USA Summary The development of the embryonic vasculature is from somatic mesoderm at the 7-somite stage to form a examined here using a monoclonal antibody, QH-1, loose plexus which moves niediad and wraps around capable of labelling the presumptive endothelial cells the developing Wolffian duct in later stages. These of Japanese quail embryos. Antibody labelling is first studies suggest two modes of origin of embryonic seen within the embryo proper at the 1-somite stage. blood vessels. The dorsal aortae and cardinal veins Scattered labelling of single cells appears ventral to the apparently arise in situ by the local segregation of somites and at the lateral edges of the anterior presumptive endothelial cells from the mesoderm. The intestinal portal. The dorsal aorta soon forms a intersomitic arteries, vertebral arteries and cephalic continuous cord at the ventrolateral edge of the vasculature arise by sprouts from these early vessel somites and continues into the head to fuse with the rudiments. There also seems to be some cell migration ventral aorta forming the first aortic arch by the 6- in the morphogenesis of endocardium, ventral aorta somite stage. The rudiments of the endocardium fuse and aortic arches. The extent of presumptive endo- at the midline above the anterior intestinal portal by thelial migration in these cases, however, needs to be the 3-somite stage and the ventral aorta extends clarified by microsurgical intervention. craniad. Intersomitic arteries begin to sprout off of the dorsal aorta at the 7-somite stage. The posterior Key words: endothelium, monoclonal antibody, cardinal vein forms from single cells which segregate vasculogenesis, QH-1, quail embryo. Introduction 1912). Subsequent minor vessels are formed by sprouting from preexisting vessels. The disadvantage The morphogenesis of the embryonic vasculature of these classic studies was that only patent vessels commences with the accumulation of presumptive could be visualized. Others have expressed the need endothelial cells (PECs) into loosely associated cords for an endothelial cell marker which could identify following their segregation from the mesoderm (re- presumptive endothelial cells just as they segregate view, Wagner, 1980). Reagen (1915) showed that from the mesoderm and begin organizing into cords blood vessels of the embryo originate within the body (e.g. Hirakow & Hiruma, 1981). The MB-1 (Peault et proper, not by invasion from the highly vascular al. 1983; Labastie etal. 1986) and QH-1 (Pardanaud et extraembryonic yolk sac. The first major blood ves- al. 1987) monoclonal antibodies fill this need as they sels, the dorsal aortae and posterior cardinal veins, label vascular endothelial cells and cells of the haema- form in situ by the segregation of mesenchymal cells topoietic lineage in embryos of the Japanese quail. from the mesoderm. This has been visualized by The sprouting form of angiogenesis has been much scanning electron microscopy (Hirakow & Hiruma, more extensively studied recently as it is the mechan- 1981; Meier, 1980). Many other vessels form by the ism by which tumours recruit a new vascular supply modification of extensive capillary plexuses as shown (Folkman, 1985). Angiogenic factors have also been by the many ink injection studies of Evans (1909, identified in developing systems. Kidney (Risau & 736 /. D. Coffin and T. J. Poole Ekblom, 1986) and brain (Risau, 1986) produce Residual unbound primary Ab was washed away with three angiogenic factors which resemble tumour angiogenic PBS changes then the secondary Ab was applied for 6-12 h factors (Shing et al. 1984; Klagsbrun & Shing, 1985). at 4°C. Any unbound secondary Ab was removed with PBS There is some controversy surrounding the origin of washes. Finally, the embryos were dehydrated in an EtOH embryonic endothelium. For example, Auerbach has series, changed to toluene and mounted on slides in proposed that the specialized endothelium of the Entellan® (VWR). brain differentiates in situ from mesenchymal stem Sections cells (Auerbach & Joseph, 1984); whereas, studies Sections were made by dissecting the embryos from the with marked cells indicate the brain endothelium yolk sac, rinsing them in PBS, then fixing them for 2h derives from the invasion of proliferating capillary minimum in Bouin's solution. After fixation, the embryos sprouts (Stewart & Wiley, 1981). Transplantations were sequentially rinsed in PBS, dehydrated in an EtOH utilizing the nuclear differences between quail and series, changed to toluene and embedded in paraffin. chick or mouse embryonic cells have revealed that the Sections were cut on a rotary microtome at 7/im and endothelium of limb buds (Jotereau & LeDouarin, mounted on albumin-coated slides. Paraffin was washed 1978; Wilson, 1983) and kidney (Ekblom et al. 1982) from the slides with toluene, then the sections rehydrated in clearly arises by invasive sprout penetration. The an EtOH series, followed by.two changes in PBS and one in segregation and directed migration of presumptive 3 % BSA for 30min. Next, the sections were stained for 2h endothelial cells and the importance of other large- in primary Ab and washed for 30min in PBS, then stained scale embryonic foldings, such as the anterior intesti- for 2h in secondary Ab and again washed in PBS. After soaking overnight at 4°C in PBS, the slides were cover- nal portal and lateral body folds, are here examined slipped with a 2 % A'-propyl gallate/80 % glycerol mixture using the monoclonal antibody QH-1 to stain quail (pH8-5) and sealed for microscopy and photography. embryos of 0-22 somites. This descriptive analysis is expanded in similar recent work (Pardanaud et al. 1987) and is a necessary prelude to an experimental Results analysis using microsurgery of the relative contri- butions of cell migration and in situ differentiation to Whole mounts and sectioned embryos were exam- the observed patterns of vascular morphogenesis. ined for immunofluorescent labelling of quail endo- Some of this work has been previously presented in thelium that highlighted the developing vasculature. abstract form (Coffin & Poole, 1986). Specifically, we studied development of the endocar- dium, the dorsal and ventral aortae, the first aortic arch, the intersomitic arteries and the cardinal veins. Materials and methods Results are summarized in Table 1. Immunocytochemistry (A) Endocardium Whole mounts and sections of Japanese quail (Coturnix Construction of the endocardium from individual coturnix japanica) were examined by using indirect immu- endothelial cells is the first step in heart development. nofluorescence to label endothelial cells. A QH-1 mono- Immunofluorescent labelling is first evident with the clonal antibody (Ab) was used first at 1:400 for whole mounts and 1:1000 for sections. This was followed by a goat appearance of PECs at the periphery of the embryo. anti-mouse FITC-conjugated IgG secondary Ab (Accurate These cells are concentrated in angiogenic sites near Biochemical, Westbury, NY) at the same concentrations as the headfold on each side of a Zacchei stage-4 the primary. Both Ab were diluted in 3 % bovine serum embryo (Fig. 1). At the 1-somite (IS) stage, the PECs albumin (BSA) in phosphate-buffered saline (PBS). begin to aggregate into capillary plexuses at the bilateral angiogenic sites and migrate mediad. Thus Whole mounts by 2S (Fig. 2), the enlarging plexuses are connected Whole mounts were prepared using techniques similar to to the extraembryonic circulation laterad, while those reported by Pardanaud et al. (1987). Embryos were mediad they grow into the pericardial coelom above removed from the yolk sac, rinsed in PBS and fixed in 4 % the anterior intestinal portal (AIP). At 2S these formalin/PBS overnight at 4°C. The fixed embryos were plexuses are considered embryonic heart primordia rinsed in PBS then permeabilized with successive changes because their location on either side of the AIP is the of (i) 30min - absolute methanol (aMeOH), (ii) 60min - aMeOH and (iii) 30min- aMeOH; all at 4 °C with constant same as the future vitelline veins and sinus venosus. agitation. After permeabilization, the embryos were rehy- The investing intraembryonic heart primordia fuse drated in an ethanol (EtOH) series (100%, 90%, 70%, at the midline of a 3S embryo. From this point of 50%, 30%, 3min each) then rinsed in PBS. Nonspecific- fusion, directly above the AIP, the ventral aorta binding sites were occupied by incubation in 3 % BSA at elongates toward the head as in a 4S embryo (Fig. 3). 4°C for 6-12h, followed by labelling of specific sites on At 6S the ventral aorta splits, and each of the two endothelial cells with the primary Ab at 4°C, 6-12 h. branches fuse with the dorsal aortae bilaterally to Quail embryonic vascular development 737 Fig. 1. A Zacchei stage-4 embryo whole mount. A cluster of PECs and individual cells are seen around the periphery of the head fold (HF) in this ventral view of the right side. Bar, 100^m. form the first aortic arches (Fig. 4). Thus by 7S, the embryonic heart lies caudal to the paired ventral aortae as the straight descending portion of a 'Y' Fig. 2. Definitive heart primordia (HP) extend medially connected at its caudal extent to the omphalomesen- through the pericardial coelom (PC) of a 2S embryo. tric or vitelline veins (Fig. 5). Notice the large PECs medially and how the HP form a From 7S to 20S, our results agree with previous diffuse capillary plexus (CP) laterally. The neural tube reports (Evans, 1912). In the area surrounding the (NT) and notochord (NC) appear as grey unlabelled pericardial coelom, large capillary strands are seen background.
Load more

Recommended publications
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Endothelium in the Pharyngeal Arches 3, 4 and 6 Is Derived from the Second Heart Field
    Thomas Jefferson University Jefferson Digital Commons Center for Translational Medicine Faculty Papers Center for Translational Medicine 1-15-2017 Endothelium in the pharyngeal arches 3, 4 and 6 is derived from the second heart field. Xia Wang Thomas Jefferson University Dongying Chen Thomas Jefferson University Kelley Chen Thomas Jefferson University Ali Jubran Thomas Jefferson University AnnJosette Ramirez Thomas Jefferson University Follow this and additional works at: https://jdc.jefferson.edu/transmedfp Part of the Translational Medical Research Commons LetSee next us page know for additional how authors access to this document benefits ouy Recommended Citation Wang, Xia; Chen, Dongying; Chen, Kelley; Jubran, Ali; Ramirez, AnnJosette; and Astrof, Sophie, "Endothelium in the pharyngeal arches 3, 4 and 6 is derived from the second heart field." (2017). Center for Translational Medicine Faculty Papers. Paper 45. https://jdc.jefferson.edu/transmedfp/45 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Center for Translational Medicine Faculty Papers by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. Authors Xia Wang, Dongying Chen, Kelley Chen, Ali Jubran, AnnJosette Ramirez, and Sophie Astrof This article is available at Jefferson Digital Commons: https://jdc.jefferson.edu/transmedfp/45 HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Dev Biol Manuscript Author .
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]