Figure 9-1: Magnetic resonance (MR) microscopy of mouse embryos at embryonic days 12.5 (A) and 9.5 (B). These embryos were perfused with BSA-DTPA-Gd, an MR contrast agent, to enhance the signal from cardiovascular structures. These volume-rendered images, based on three-dimensional T1-weighed scans, demonstrate the cardiac chambers, cardiac valves, aortic arches, intersegmental vessels, cranial vasculature, and hepatic vasculature. Scale bars are marked as 2 mm or 1 mm. Rt = right. (Data courtesy of Brad Smith, University of Michigan.)
Figure 9-2: The postgastrulation morphogenetic events involved in the formation of the tubular heart. The upper panel represents a chick embryo at stage 7/8 H/H, demonstrating the emergence of endocardial precursor mesenchymal cells from the splanchnic mesoderm, which gives rise to the future myocardium. It is proposed that the formation of both endocardium and myocardium is induced by adjacent endoderm. The lower panel shows that subsequent to the migration and assembly of endocardial precursor mesenchymal cells during stages 7-8 H/H, the cellular plexus coalesces to form the definitive endocardial tube enveloped by the myocardial tube. Note that the endocardium is still in close proximity to the ventral side of the foregut. (Courtesy of Yukiko Sugi, Cardiovascular Developmental Biology Center, Medical University of South Carolina.) Figure 9-3: A lateral plate of mesoderm on each side of the midline forms the progenitor for the development of the heart and portions of the great vessels. The NK-Factor homeobox genes, such as Nkx2.5, in combination with multiple other genes, such as the serum response factor (SRF), are responsible for activating commitment of these undifferentiated cells to cardioblasts. Myocyte enhancer factor (MEF) has a binding site in practically all muscle genes and is essential to the development of cardiac myocytes. The CARP gene is downstream of Nkx2.5 in the cardiac lineage. The genes responsible for the fusion of the two lateral mesodermal plates into a single tube are unknown, but experiments show that GATA-4 is necessary, along with SRF and many other genes yet to be identified. Genes involved in laterality include Activin, FGF-9, Shh, and nodal. The cardiac tube that forms a loop to the right requires Nkx genes and the eHAND and dHAND as well as inv (inversion of embryonic turning) and iv genes. The dHAND gene is responsible for the formation of the right ventricle, and the eHAND for that of the left ventricle.
Figure 9-4: Schematic ventral dissections of human embryos of different ages, showing formation of the heart loop. (Adapted from Davis CL. Development of the human heart from its first appearance to the state found in embryos of 20 paired somites. Contrib Embryol 1927; 19:245. Reproduced with permission from the Carnegie Institution of Washington.)
Figure 9-5: Schematic representation of the tubular heart during looping. Panel A depicts an inferior view of the heart, while panel B represents a superior view. Note that at this stage (approximately 4 weeks of development in the human), all the segments are more or less arranged in series. From inflow to outflow: V = sinus venosus; RA = right atrium; LA = left atrium; AVC = atrioventricular canal; LV = left ventricle; RV = right ventricle; OFT = outflow tract.
' Figure 9-6: Schematic representation of the location of the so-called primary ring (characterized by the expression of the antigen GlN2) in different stages of human development. The drawings illustrate the development of the conduction system as a derivative of the primary ring but also show that the changes in the topography of the ring tissue reflects (1) the rightward expansion of the atrioventricular canal and (2) the leftward shift ("wedging") of the developing aorta. 1 = "primary ring"; 2 = right atrioventricular ring; 3 = atrioventricular nodal area; 4 = penetrating His bundle; 5 = crest of interventricular septum; 6 = septal branch; 7 = retroaortic branch. Areas indicated with an asterisk have lost their expression. The Carnegie stages of development presented in the drawings a to d are a = stage 14; b = stage 15; c = stage 17; d = stage 18-19. (Adapted from Wessels et al.125)
' Figure 9-7: Schematic representation of the localization of remnants of the primary ring in the neonatal human heart. The ring is projected on a superior view of the aortic mitral fibrous unit of the adult heart. The black dots indicate the areas in which remnants of the ring are detected in a series of neonatal hearts. 1 = anterolateral part of the right atrioventricular ring; 2 = posteromedial part of the right atrioventricular ring; 3 = "deadend" tract of the conduction axis; 4 = lateral part of the retroaortic rootbranch; 5 = posterior part of the retroaortic rootbranch. AVN = atrioventricular node; AoV = semilunar valve of the aorta; LBB = left bundle branch; mi = mitral valve; PuV = semilunar valve of the pulmonary trunk; Rbb = right bundle branch; SB = septal branch; tri = tricuspid valve. (Adapted from Wessels et al.126)
' Figure 9-8: Schematic representation of myocardial trabecular development in the chick embryo. A. At the onset of ventricular trabeculation [around Hamburger-Hamilton (HH) stage 17], the process is limited to the primitive ventricle (V), while the inner curvature of the cardiac loop remains smooth. B. Transverse and frontal sections that show the distribution of secondary trabeculae (around HH stage 28). C. Mature tertiary trabecular pattern (HH stage 45). Only two of the principal bundles are shown in the left ventricle for clarity. In both ventricles, the trabeculae are arranged in a counterclockwise apicobasal spiral (viewed from base to apex). Differences between the right and left ventricles relate primarily to geometric differences (cone/crescent versus cylinder/prolate ellipsoid). Ct = conotruncus; At = primitive atrium. (Adapted from Sedmera et al.144)
' Figure 9-9: Posterior view of the atria and sinus venosus in embryos. A. 3-mm CR length; B. 5-mm CR length; C. 12-mm CR length. D. Newborn. Diagrammatic. A(C)CV = anterior (common) cardinal vein; AV = azygos vein; CS = coronary sinus; IVC = inferior vena cava; PCV = posterior cardinal vein; PV = pulmonary vein; SH = sinus horn; UV = umbilical vein; VM = vein of Marshall; VV = vitelline vein. (From Van Mierop LHS, Wiglesworth FW. Isomerism of the cardiac atria in the asplenia syndrome. Lab Invest 1962; 11:1303. Copyright by U.S. and Canadian Academy of Pathology.)
' Figure 9-10: A model for the development of the atrial septal complex in the human heart. Panels A-C of this cartoon illustrate the key events in the formation of the primary atrial septum (A-C). Panel Dschematically depicts the formation of the atrial septum and venous valves. Panel A represents a heart at approximately 4% weeks of development. The AV cushions can be distinguished but have not yet fused. The leading edge of the primary septum is covered by a mesenchymal cap which is in continuity with the dorsal mesenchymal protrusion of the dorsal mesocardium. Panel B represents the situation at approximately 6 weeks of development. The leading edge of the primary atrial septum, covered with a mesenchymal cap, is now approaching the AV cushions, which are in the process of fusing. Within the myocardial portion of the primary septum, multiple fenestrations represent the developing secondary foramen. Completion of fusion of the mesenchymal tissues at 6 to 7 weeks of development (panel C) results in the closure of the primary interatrial foramen. At this time, a prominent secondary foramen can be found within the superior portion of the primary septum. The cartoon in panel D shows how the secondary atrial septum is formed as a result of infolding of the atrial roof. This occurs at the margin between the myocardium and the left and right atrial expression domain. The myocardium of the primary atrial septum is part of the left atrial expression domain; the orifice of the pulmonary vein also is surrounded by myocardium with a left atrial molecular phenotype. This panel also illustrates that based on the gene expression patterns, the left venous valve develops as a myocardial structure with a right atrial molecular phenotype, whereas the right venous valve (just like the secondary atrial septum) develops by infolding, in this case of the junctional tissue between the right atrium and the sinus venosus. iAVC = inferior atrioventricular cushion; sAVC = superior atrioventricular cushion; DM = dorsal mesocardium; DMP = dorsal mesenchymal protrusion; pf = primary foramen; PS = primary atrial septum; sf = secondary foramen; LA = left atrium; RA = right atrium; OF = oval fossa; pAS = primary atrial septum; sAS = secondary atrial septum; PuV = pulmonary vein; LVV = left venous valve; RVV = right venous valve (From Wessels et al.139)
Figure 9-H: Schematic drawing of some of the developmental events involved in the septation of the outflow tract. Panel A depicts the stage in which the endocardial cushion tissues in the outflow tract (conal cushions and truncal swellings) and the aorticopulmonary septum have not yet fused. Panel B illustrates that the truncal swellings contribute to the formation of the semilunar valves of the aorta and the pulmonary trunk, whereas the fusing conal cushions are forming the mesenchymal outlet septum. At this stage, the conal myocardium starts to myocardialize the outlet septum. Panel C shows one of the final stages. The aorticopulmonary septum has now completely separated the aorta and pulmonary trunk above the level of the semilunar valves, while below the valves the outlet septum divides the outlet segment of the heart in a subaortic and subpulmonary outlet.
' Figure 9-42: Schematic drawings of the formation of the atrioventricular junction in the human heart. A. The situation at the atrioventricular junction at 4 to 5 weeks of development. Myocardial continuity between atrium and ventricle occurs through the myocardium of the atrioventricular canal. The AV junction is sandwiched between the tissues of the AV sulcus at the epicardial side and the AV cushion at the endocardial side. B. With progressive remodeling of the AV junction, the sulcus tissues expand toward the midline of the AV canal as the cushion tissue remodels. C. With completion of this process, continuity is lost between atrial and ventricular myocardium. A = atrium; V = ventricle; ST = sulcus tissue; AV = myocardium of the atrioventricular canal; CT = cushion tissue. (Adapted from Wessels et al.148)
' Figure 9-43: Development of the aortic arch system. Embryos of (A) 3 mm, (B) 4 mm, (C) 40 mm, (D) 44 mm, (E) 47 mm, (F) neonate. (Adapted from Congdon ED. Transformation of the aortic arch system during the development of the human embryo. Contrib Embryol 1922; 14:47.)
' Figure 9-H: Expression of neuromuscular markers in the developing vertebrate heart. Panel A shows a transverse section of a human heart at 6 weeks of development immunohistochemically stained for the presence of a carbohydrate moiety recognized by the monoclonal antibody GlN2 (see also Wessels et al.425). The section shown in panel B is from a rabbit embryo at 45 days of development and is immunohistochemically stained for the presence of neurofilaments (Wessels et al.439). RAVR = right atrioventricular ring bundle; His = bundle of His; LBB = left bundle branch; RBB = right bundle branch.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.