Placenta and Placental Nutrition of the Embryo
The placenta (from Greek plakuos, flat cake) is an organ created from the zygote that links two individuals, the mother and the fetus. Throughout the pregnancy, placental mass maintains a dynamic relationship with the weight of developing fetus. The placenta serves to attach the embryo-fetus to the uterine wall and to exchange nutrients, wastes, and gases between the maternal blood and the embryo-fetal blood. It also provides endocrine and immune support for the developing fetus.
The placenta forms by the differentiation of the trophoblast (the outer cell mass of the early embryo that gives rise to the placenta) in two different layers, the cytotrophoblast (mitotically active) and the syncytiotrophoblast (lacunas forming tissue able to fuse the placenta to the wall of the uterus). The placental anatomy is comprised of the placental parenchyma, umbilical cord, and amnion, all of which have specific macroscopic and microscopic features.
The full-term human placenta is a disk-like round organ weighing approximately 1 lb. (approximately 450 g) at delivery that is formed by a chorionic plate and a basal plate. The chorionic plate is a fibrous disc into which two umbilical arteries (sometimes one) coming from the embryo-fetal district ramify as chorionic plate vessels, each penetrating the plate to enter the stem of a villous tree. A vein draining oxygenated blood accompanies each arterial vessel back toward a single umbilical vein. The chorionic plate is covered by the amniotic membrane. The basal plate (maternal surface) is composed of 10-40 islands of parenchyma called cotyledons, subdivided by an incomplete system of septa. Cotyledons and septa are generated during the placental growth as the gestation progresses due to the relative lack of space in the uterine cavity. The basal plate is composed of a mixture of trophoblastic and decidual cells embedded in extracellular debris as well as blood clot. The placental parenchyma is composed of a highly vascularized stromal compartment lined or covered by trophoblast. The stroma is mesoderm filled with vascular and lymphatic vessels. The trophoblast expresses unique antigens (HLA-G and Fas ligand) that promote its graft-like immunological acceptance (tolerance) by the antigenically dissimilar maternal host.
From the microscopic point of view, it is essential to refer to the placental villous system development. At two weeks gestation, in the lacunar spaces, formed by the rapid expansion of the syncyziotrophoblast, finger-like columns of the proliferating cytotrophoblasts form the primary villi. At 3 weeks gestation, extra-embryonic mesenchyme, the future connective tissue of the placenta, grows into the center of the villi that are now called secondary villi. Successively, the mesenchyme differentiates into blood vessels and cells, forms an arteriocapillary network fused with placental vessels, and yields, at 4 weeks, the formation of the tertiary villi. Five types of villi have been detected on the basis of their size, stromal characteristics and vessel structure: (1) Stem villi give mechanical support to the villous trees. They have a dense fibrous stroma with relatively large vessels that are centrally located. (2) Long slender mature intermediate villi arise from the ends of stem villi. They have a loose stromal core, with small arterioles and capillaries. (3) Terminal villi are the final branches of the villous tree. They have an extensive system of capillaries and an inhomogeneous thickness of the trophoblast. In some area, trophoblast is reduced just to a thin layer known as vasculosyncytial membrane. The proportion of villus surface occupied by the vasculosyncytial membrane increases with the gestational age. (4) Immature intermediate villi, usually present at the central area of the lobule, are recognized because of the presence of several macrophages (Hofbauer cells). (5) Mesenchymal villi are immature villi present at the beginning of the gestation usually confined on the surface of immature intermediate villi as the pregnancy progresses.
In all mammalian species, nutrition of the conceptus is initially histiotrophic with the growing and rapidly dividing trophoblast deriving nutrients from simple diffusion and from phagocytosing maternal tubal and uterine secretions; following implantation and establishment of the placenta there is a transition to hemotrophic nutrition, with exchange between maternal and embryofetal blood circulations.
A possible histiotrophic pathway during early pregnancy has been extensively described. It involves the secretions from the uterine glands that are known to enter the intervillous space. The maternal secretions are taken up by the trophoblast and locally digested or diffuse throughout the villus mesenchyma along the stromal channels into the coelomic fluid. Finally, they are absorbed by the epithelia of the yolk sac and pass to the embryo though the vitelline circulation (the earliest embryonal circulation). At early stages of pregnancy, the yolk sac has a determinant role in delivering the nutrients because its vascularization is much more developed than that of the villous system. Histiotrophic nutrition benefits the embryo especially during embryogenesis because it reduces the risk to high oxygen exposure. Support for this theory comes from the observations that known teratogens as well as thalidomide and ethanol disrupt normal developmental patterns through the formation of elevated levels of free radicals (reactive oxygen species).
Hemotrophic nutrition takes place when the two different sides, both maternal and fetal, create a complex circulation. The maternal or intervillous placental circulation proceeds as the trophoblastic shell invades the uterine stroma to reach the maternal capillaries. Fetal circulation arises from the stroma of the villi when they begin to organize a primitive capillary system that connects to the intrafetal circulation. Toward the end of the first trimester both fetal and maternal circulation results in a hemochorial arrangement where maternal and fetal blood ideally are separated by a barrier. Maternal nutrients cross the intervillous space, trophoblast cells, the fibrous core of the villus, and the endothelial cells of the fetal capillaries to enter the fetal blood. Wastes from the fetus move in the opposite direction.
Nutrition of the embryo and fetus is mediated by very complex systems of transport, the maternal-fetal exchange. Placenta has several mechanisms of transport including simple diffusion (small molecules like oxygen, water, CO2 move along concentration gradients from higher to lower concentrations), facilitated diffusion where carrier molecule dependent diffusion also moves molecules such as glucose along concentration gradients from higher to lower concentrations) dependent on local concentration gradients, needs a carrier molecule), and active transport against a concentration gradient. Active transport utilizes ATP and is therefore ATP dependent. Active transport is required to move amino acids, calcium, iron, and some water-soluble vitamins.
Glucose is the major metabolic "fuel" for the embryo and fetus (and placenta). Specific glucose transporters named GLUT 1 (much more widespread) and GLUT 3 (more vessels specific) are present on plasma membranes of placental barriers facing the maternal and fetal sides. Proper glucose uptake is achieved through a lower fetal glucose concentration, which increases the transplacental glucose gradients. With the advance of gestational age, in normal pregnancy, the glucose concentration decreases in the fetal blood despite the fact that in the maternal blood it remains constant.
The transport of aminoacids across the placenta is active and involves three fundamental steps. First, the uptake from maternal circulation across the microvillus membrane. Second, the transport throughout the trophoblast cytoplasm. Third, the transport across the basal membrane and into the umbilical circulation. A number of different variations of amino acid transport systems exist. For example, neutral aminoacids as well as glycine and alanine are transported by means of at least six different systems. It is worth noting how the serine is not transported from the maternal to the fetal circulation and some of its production occurs in the fetal liver derived from the glycine. Also is important the exchange of glutamine and glutamate performed by the placenta-fetal liver interaction. In particular, the fetal liver takes up glutamine and releases glutamate.
The placenta has a considerable capacity for lipid uptake and transport. Several lipase activities are involved in such a mechanism. Most of the transport involves the breakdown of triglycerides to free fatty acids and glycerol and re-esterification with intracellularly generated glycerol phosphate on the fetal side. Again, a direct passage of free fatty acids is also possible, and, although the fetus has an internal (endogenous) source of cholesterol, there is evidence that yolk sac and placenta take up maternal cholesterol in the form of LDL and HDL Fetal lipid metabolism is essential for the rapid fetal growth and cholesterol, in particular, is needed for a normal development.
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