Transfer of 125I-Labelled Lysozyme from the Maternal into the Fetal Circulation in Rabbits and Mice

2015 ◽  
pp. 382-390
Author(s):  
A. Glynn ◽  
M. Adinolfi
Keyword(s):  
Fetal Circulation

The basics of fetal circulation and echocardiography

Choonpa Igaku ◽  
2015 ◽  
Vol 42 (4) ◽  
pp. 457-473
Author(s):  
Masaki NII
Keyword(s):  
Fetal Circulation

scholarly journals Molecular Mechanisms Underlying Remodeling of Ductus Arteriosus: Looking beyond the Prostaglandin Pathway

2021 ◽  
Vol 22 (6) ◽  
pp. 3238
Author(s):  
Ho-Wei Hsu ◽  
Ting-Yi Lin ◽  
Yi-Ching Liu ◽  
Jwu-Lai Yeh ◽  
Jong-Hau Hsu
Keyword(s):  
Adverse Effect ◽  
Clinical Management ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Surgical Intervention ◽  
Ductus Arteriosus ◽  
Clinical Problem ◽  
Cyclooxygenase Inhibitors ◽  
Medical Patients ◽  
Fetal Circulation

The ductus arteriosus (DA) is a physiologic vessel crucial for fetal circulation. As a major regulating factor, the prostaglandin pathway has long been the target for DA patency maintenance or closure. However, the adverse effect of prostaglandins and their inhibitors has been a major unsolved clinical problem. Furthermore, a significant portion of patients with patent DA fail to respond to cyclooxygenase inhibitors that target the prostaglandin pathway. These unresponsive medical patients ultimately require surgical intervention and highlight the importance of exploring pathways independent from this well-recognized prostaglandin pathway. The clinical limitations of prostaglandin-targeting therapeutics prompted us to investigate molecules beyond the prostaglandin pathway. Thus, this article introduces molecules independent from the prostaglandin pathway based on their correlating mechanisms contributing to vascular remodeling. These molecules may serve as potential targets for future DA patency clinical management.

Persistent Pulmonary Hypertension of the Newborn

1991 ◽  
Vol 7 (S1) ◽  
pp. 66-69
Author(s):  
George Lister
Keyword(s):  
Pulmonary Hypertension ◽  
Diaphragmatic Hernia ◽  
Vascular Development ◽  
Clinical Syndrome ◽  
Persistent Pulmonary Hypertension ◽  
Maternal Infection ◽  
Fetal Circulation ◽  
Cns Disease ◽  
Persistent Fetal Circulation

Persistent pulmonary hypertension of the newborn or persistent fetal circulation is a clinical syndrome that is usually apparent within the first 2 days after birth because of the presence of hypoxemia (2;12;19). The syndrome was first described in an abstract by Gersony, Due, and Sinclair (6) in 1969. Two infants were reported who had “RV decompensation, cyanosis and clear lung fields… in the absence of recognizable cardiac, pulmonary, hematologic or CNS disease.” The syndrome has been associated with aspiration of meconium, diaphragmatic hernia, asphyxia, hemorrhage, shock, and maternal infection (4;18). In other cases, there is no clear antecedent event. Despite considerable interest in the problem and a wealth of research related to pulmonary vasoregulation and vascular development in the fetus and newborn, the etiology of the syndrome remains obscure 20 years since its recognition.

Infants With Severe Respiratory Failure and Persistance of the Fetal Circulation, Without Hyperventilation

PEDIATRICS ◽  
1986 ◽  
Vol 78 (2) ◽  
pp. 379-379
Author(s):  
DANIEL L. LEVIN
Keyword(s):  
Respiratory Failure ◽  
Treatment Plan ◽  
General Treatment ◽  
Control Group ◽  
Prospective Analysis ◽  
Severe Respiratory Failure ◽  
Fetal Circulation

To the Editor.— I just finished reading the article by Wung et al Pediatrics 1985;76:488-494). I was quite surprised at the publication of this article. There are several problems that make it such that I question its appropriateness in the article section of Pediatrics. The most important objection is that it is a retrospective collection of patients who were treated by some general treatment plan with no prospective analysis or control group. The data collected are dubious at best; for example, the authors do not state where the O2 samples were drawn and they do not define what they mean by the patient's oxygenation being improved with tolazoline.

Biotin transport in microvillous membrane vesicles, cultured trophoblasts, and isolated perfused human placenta

1992 ◽  
Vol 262 (2) ◽  
pp. C302-C308 ◽  
Author(s):  
P. I. Karl ◽  
S. E. Fisher
Keyword(s):  
Membrane Potential ◽  
Growth And Development ◽  
Membrane Vesicles ◽  
Tissue Analysis ◽  
Michaelis Constant ◽  
Fetal Circulation ◽  
Maximal Stimulation ◽  
Placental Transport ◽  
Biotin Molecule ◽  
Microvillous Membrane Vesicles

Biotin, essential for normal fetal growth and development, must be transported across the placenta to reach the fetus. This study evaluated placental transport of biotin using microvillous membrane vesicles (MMV), cultured trophoblasts, and isolated perfused cotyledon. Biotin uptake in MMV was stimulated by an inward Na+ gradient. In the presence of Na+, maximal stimulation was observed with Cl-, among various anions. Biotin uptake required 1 Na+ per biotin molecule. Kinetic analysis in MMV showed saturable transport with a Michaelis constant (Km) of 26.1 +/- 2.9 microM. Increases in membrane potential did not alter biotin uptake. Biotin uptake by cultured trophoblasts was also stimulated in the presence of Na+ and was saturable (Km = 7.0 +/- 1.5 microM). In the perfused placental cotyledon, maternal-to-fetal (M-to-F) biotin transfer was not saturable. However, biotin transfer in the M-to-F direction was significantly greater than the reverse. When the fetal circulation was closed to allow accumulation, an F/M ratio of only 1.056:1 was achieved. Tissue analysis of biotin contents suggested an active accumulation within the placental compartment. This study demonstrates that biotin is actively transported into the placenta, across the microvillous membrane, and released into the fetal compartment at a slower rate.

Fetal Circulation Times and their Implications for Tissue Oxygenation

1975 ◽  
Vol 6 (6) ◽  
pp. 342-355 ◽  
Author(s):  
Gordon G. Power ◽  
Lawrence D. Longo
Keyword(s):  
Tissue Oxygenation ◽  
Fetal Circulation
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