this unit covers some basic ideas in early cardiovascular development. the first section focuses on the development of blood and blood vessels: blood production starts mainly in the yolk sac and moves to the liver/spleen, then to the bone marrow during development and involves differentiation of hemangioblast cells. these cells are derived from mesenchymal cells and triggered by the growth factor FGF to differentiate into blood cell precursors, hematopoetic stem cells, or blood vessel (capillary) walls, which then converge into larger and larger vessels. VEGF is a growth factor that stimulates nearby mesenchyme cells to differentiate into smooth muscle or pericyte cells.
the next sections describe the early structural development of the heart. the formation of the heart chambers begins when the endocardial cushion forms in the middle of the heart via a fusion of projections of tissue from the anterior and posterior walls. in the atriums, the primary septum is formed with a secondary foramen, and the secondary septum is formed with a foramen ovale. in the prenatal heart, blood flows from the right atrium, into the foramen ovale, through the primary septum, directly into the left atrium, bypassing the lungs. (this is the second "shunting" we've learned about- the first being the ductus arteriosus) in the post natal heart, the pressure from the pulmonary artery in the left atrium causes the primary septum to close and fuse with the secondary, creating the fossa ovalis. the ventricles are partitioned when the muscular and the membranous aspects of the interventricular septum join, closing up the interventricular foramen. finally, the endocardial cushion projects a spiral aortic pulmonary septum that projects into the bulbus cordis / truncus arteriosus vessel and separates it into the aortic and pulmonary trunks. the points of fusion between the bulbus cordis and truncus arteriosus becomes the semilunar valves.
we then look at some defects possible in the development of these structures. in the atriums, atrial septal defect can occur, called probe patent formation, when there is an imperfect adhesion between the primary and secondary septums. in the ventricles, VSD can occur when the membranous aspect of the interventricular septum does not close completely.
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