Fetal Physiology

2020 ◽  
pp. 92-97
Author(s):  
Anita Pawar
Keyword(s):  
Fetal Physiology

scholarly journals A Potential Role and Contribution of Androgens in Placental Development and Pregnancy

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 644
Author(s):  
Agata M. Parsons ◽  
Gerrit J. Bouma
Keyword(s):  
Fetal Development ◽  
Fetal Loss ◽  
Membrane Receptors ◽  
Placental Development ◽  
Placental Function ◽  
Fetal Physiology ◽  
Estrogen Synthesis ◽  
And Function ◽  
Pregnancy Disorders

Successful pregnancy requires the establishment of a highly regulated maternal–fetal environment. This is achieved through the harmonious regulation of steroid hormones, which modulate both maternal and fetal physiology, and are critical for pregnancy maintenance. Defects in steroidogenesis and steroid signaling can lead to pregnancy disorders or even fetal loss. The placenta is a multifunctional, transitory organ which develops at the maternal–fetal interface, and supports fetal development through endocrine signaling, the transport of nutrients and gas exchange. The placenta has the ability to adapt to adverse environments, including hormonal variations, trying to support fetal development. However, if placental function is impaired, or its capacity to adapt is exceeded, fetal development will be compromised. The goal of this review is to explore the relevance of androgens and androgen signaling during pregnancy, specifically in placental development and function. Often considered a mere precursor to placental estrogen synthesis, the placenta in fact secretes androgens throughout pregnancy, and not only contains the androgen steroid nuclear receptor, but also non-genomic membrane receptors for androgens, suggesting a role of androgen signaling in placental function. Moreover, a number of pregnancy disorders, including pre-eclampsia, gestational diabetes, intrauterine growth restriction, and polycystic ovarian syndrome, are associated with abnormal androgen levels and androgen signaling. Understanding the role of androgens in the placenta will provide a greater understanding of the pathophysiology of pregnancy disorders associated with androgen elevation and its consequences.

Fetal physiology cardiotocography training, a regional evaluation

2020 ◽  
pp. 102039
Author(s):  
Li-Anne Zhu ◽  
Julie Blanc ◽  
Hélène Heckenroth ◽  
Caroline Peyronel ◽  
Blanche Graesslin ◽  
...  
Keyword(s):  
Fetal Physiology

Fetal physiology

2015 ◽  
pp. 408-415
Author(s):  
David Chambers ◽  
Christopher Huang ◽  
Gareth Matthews
Keyword(s):  
Fetal Physiology

Special Susceptibility of the Fetal and Neonatal Hematopoietic System to Chemical Pollutants Including Drugs Administered to the Mother

PEDIATRICS ◽  
1974 ◽  
Vol 53 (5) ◽  
pp. 816-817
Author(s):  
Audrey K. Brown
Keyword(s):  
Aplastic Anemia ◽  
Good Evidence ◽  
Red Cells ◽  
Coagulation System ◽  
Hematopoietic System ◽  
Chemical Effects ◽  
Fetal Physiology ◽  
Environmental Agents ◽  
Physiologic Maturity ◽  
The Impact

Because of the anemia or bleeding that may herald the adverse impact of any agent upon the hematopoietic system, the capacity of drugs, insecticides, lead, and other agents to cause malfunction of this system has long been recognized. As a matter of fact, the major therapeutic step in the management of recognized aplastic anemia is to separate the child from his environment even before the offending agent has been identified. There is, however, no good evidence to date that the child or neonate is singularly susceptible to aplastic anemia or neutropenia from such agents. In response to other agents, there is a special susceptibility of the hematopoietic system in the fetus and newborn. One special feature of the fetus affecting susceptibility to environmental agents is that, in a sense, he is trapped in his environment; and, we cannot extract him early enough from exposures via the mother and placenta. The smoking mother, the heroin addict, and the mother exposed to industrial pollutants are the conduits through whom poisons may reach the fetus. The special features of fetal physiology, the stage of organ development, and the phase of physiologic maturity dictate the uniqueness of response at a particular time in gestation or immediately after delivery. CHEMICAL EFFECTS ON RED CELLS OR PLATELETS In the last trimester women take an average of 8.7 drug agents or vitamins and 80% of these agents are taken without medical supervision. The impact of these agents on red cells, white cells, platelets, the fetal coagulation system, and on the appearance of pigments formed during red cell destruction are in some instances predictable because of the growing fund of information concerning the unique physiology of these cells and systems in the fetus and newborn.

Back from the brink: a reversible cardiac cause of fetal hydrops

2020 ◽  
pp. 1-12
Author(s):  
David Lloyd ◽  
John Simpson ◽  
Vita Zedere
Keyword(s):  
Fetal Outcome ◽  
Fetal Hydrops ◽  
Management Options ◽  
Fetal Physiology ◽  
Wide Range ◽  
Term Delivery ◽  
Echocardiographic Assessment ◽  
Long Term Prognosis ◽  
Full Term Delivery

Fetal hydrops is a form of cardiovascular decompensation unique to fetal physiology, with a wide range of potential causes. In many conditions, it is associated with poor fetal outcome. This chapter explores a challenging case of fetal hydrops, discussing differential diagnoses, methods of echocardiographic assessment, and potential management options. Successful identification and treatment of the underlying cardiac disorder in this case led to complete resolution of hydrops, allowing for full-term delivery, with a good long-term prognosis.

scholarly journals The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

2002 ◽  
Vol 174 (1) ◽  
pp. 27-36 ◽  
Author(s):  
EC Jensen ◽  
BW Gallaher ◽  
BH Breier ◽  
JE Harding
Keyword(s):  
Blood Pressure ◽  
Fetal Growth ◽  
Amino Nitrogen ◽  
Late Gestation ◽  
Heart Weight ◽  
Fetal Sheep ◽  
Fetal Physiology ◽  
Endocrine Status ◽  
Nitrogen Concentrations ◽  
The Right

Exposure of the fetus to excess maternal glucocorticoids has been postulated to alter fetal growth and development, and thus provide a possible mechanism for the link between impaired fetal growth and altered postnatal physiology. However, the effects of exposure to excess maternal glucocorticoids on fetal physiology and metabolism in utero have not been described. We therefore studied the effects of chronic maternal cortisol infusion on fetal growth, blood pressure, metabolism and endocrine status in chronically catheterised fetal sheep. We infused hydrocortisone (80 mg/day, n=6) or saline (n=8) for 10 days into the pregnant ewes beginning at 119 days of gestation. Maternal cortisol infusion reduced fetal growth rate by 30% (girth increment 2.9+/-0.3 vs 1.8+/-0.4 mm/day, P=0.03). Maternal cortisol infusion increased fetal heart weight by 15% relative to body weight and increased ventricular wall thickness by 30% in the left and 50% in the right ventricle. The weight of the spleen was reduced by 30% and placental weight reduced by 25%. Fetal blood pressure increased by approximately 10 mmHg (20%) during maternal cortisol infusion. Maternal cortisol infusion did not alter amino-nitrogen concentrations. However, maternal lactate concentrations increased by 80% and fetal lactate concentrations increased by 74% with maternal cortisol infusion, and both maternal and fetal urea concentrations increased by 40%. Circulating maternal IGF-binding protein (IGFBP)-3 levels had increased by 20% by the end of the maternal cortisol infusion. Fetal IGF-I concentrations decreased during cortisol infusion and fetal IGFBP-1 concentrations were negatively correlated with fetal weight (r=-0.76, P=0.02). We conclude that even a modest elevation of maternal cortisol levels affects fetal growth, cardiovascular function, metabolism and endocrine status which may have long-term consequences.

Epigenetic regulation of placental endocrine lineages and complications of pregnancy

2013 ◽  
Vol 41 (3) ◽  
pp. 701-709 ◽  
Author(s):  
Rosalind M. John
Keyword(s):  
Genomic Imprinting ◽  
Giant Cells ◽  
In Utero ◽  
Imprinted Genes ◽  
Endocrine Organ ◽  
Fetal Physiology ◽  
Trophoblast Giant Cells ◽  
In Utero Development ◽  
Genetic Conflicts

A defining feature of mammals is the development in utero of the fetus supported by the constant flow of nutrients from the mother obtained via a specialized organ: the placenta. The placenta is also a major endocrine organ that synthesizes vast quantities of hormones and cytokines to instruct both maternal and fetal physiology. Nearly 20 years ago, David Haig and colleagues proposed that placental hormones were likely targets of the epigenetic process of genomic imprinting in response to the genetic conflicts imposed by in utero development [Haig (1993) Q. Rev. Biol. 68, 495–532]. There are two simple mechanisms through which genomic imprinting could regulate placental hormones. First, imprints could directly switch on or off alleles of specific genes. Secondly, imprinted genes could alter the expression of placental hormones by regulating the development of placental endocrine lineages. In mice, the placental hormones are synthesized in the trophoblast giant cells and spongiotrophoblast cells of the mature placenta. In the present article, I review the functional role of imprinted genes in regulating these endocrine lineages, which lends support to Haig's original hypothesis. I also discuss how imprinting defects in the placenta may adversely affect the health of the fetus and its mother during pregnancy and beyond.

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