Fetal circulation

Since propranolol crosses the placenta and enters the fetal circulation, fetal cardiac responses to the stresses of labor and delivery will be blocked. Additionally, propranolol crosses the blood-brain barrier and is associated with mood changes and depression. School difficulties are commonly associated with its use in children. Propranolol may also cause hypoglycemia in infants. 

M3. Maner, F. D., Saffan, B. D., Wiggins, R. A., Thompson, J. D., and Preedy, J. R. K., Interrelationship of estrogen concentrations in the maternal circulation, fetal circulation and maternal urine in late pregnancy. J. Clin. Endocrinol. Metab. 

In liver tissues deoxycorticosterone is reduced very extensively to its tetrahydro derivatives both isomers (3a,5/3 and 3/3,5a) have been detected. Moreover, circulating fetal deoxycorticosterone can be converted to corticosterone in fetal adrenals (Pasqualini et al., 1970b). 

Circulating fetal corticosterone is also converted into tetrahydrocorti-costeronc , 20d-dihydroeorticosteroii( , 6 8-hydroxycorticosterone, and principally into its 11-kcto derivative, 11-dohydrocorticosteronc. This la. t transformation is particularly notable in the lungs (Pasqualini et ai., lt)69a). 

Treatment of pregnant women with warfarin can lead to fetal bone abnormalities (fetal warfarin syndrome). Two proteins are present in bone that contain y-carboxygluta-mate, osteocalcin and bone matrix Gla protein. Osteocalcin also contains hydroxyproHne, so its synthesis is dependent on both vitamins K and C in addition, its synthesis is induced by vitamin D. The release into the circulation of osteocalcin provides an index of vitamin D stams. 

Placental transfer of trichloroethylene occurs in animals. Trichloroethylene inhaled by pregnant sheep and goats, at levels used to induce analgesia and anesthesia, is rapidly distributed into the fetal circulation, with peak levels occurring approximately 40-50 minutes after maternal exposure (Helliwell and Hutton 1950). The concentration of trichloroethylene in umbilical vein blood was comparable to that found in the maternal carotid artery. 

Reik We think it is an indirect effect. We have measured IGF2 transcription and peptide in the fetal circulation. This is normal. The only thing that is missing is the Igf2 transcript which is specific to the placenta. The placenta is small from about Day 13. The fetus shows much more protracted growth deficiency only on Day 17—18 can you see the fetus slow down. 

Rh incompatibility may occur when an Rh negative mother carries an Rh-positive fetus. At the time of delivery, a small amount of the baby s Rh-positive blood may gain access to the maternal circulation. In response, the immune system of the mother produces anti-Rh antibodies. During the subsequent pregnancy, the fetus is exposed to these antibodies as they cross the placenta. If this fetus is also Rh-positive, then the anti-Rh antibodies attack the fetal erythrocytes and cause hemolytic disease of the newborn (erythroblastosis fetalis). This may occur in about 3% of second Rh-positive babies and about 10% of third Rh-positive babies. The incidence continues to increase with subsequent pregnancies. 

We have determined thiamine levels of mother and infant at parturition (Bll). Thiamine in the fetal circulation is 5 times higher than in the mother s. A similar situation exists in the guinea pig (B35). 

Since transport across the syncytiotrophoblast layer is the rate-limiting step in the absorption of substances from the maternal circulation to the fetal, these cells can provide information on uptake processes which are subject to intracellular regulatory mechanisms or affected by intracellular metabolism. However, it is very difficult to isolate this layer because of its syncytial nature. As a result, the undifferentiated precursor cytotrophoblast cells have been isolated and cultured. These cells do not proliferate in culture, but aggregate and spontaneously differentiate into syncytiotrophoblasts [49],... 

K.E. Schmid, W.S. Davidson, L. Myatt, and L.A. Woollett. Transport of cholesterol across a BeWo cell monolayer Implications for net transport of sterol from maternal to fetal circulation. J Lipid Res. 44 1909-1918 (2003). 

A similar adaptive mutation is found in human fetal hemoglobin. This has a lower oxygen affinity than the adult in the absence of phosphate, but it also has a lower affinity for DPG, due mainly to the replacement His H21(143)/3 — Ser. As a result, the oxygen affinity of fetal blood exceeds that of the adult, which helps the transfer of oxygen from the maternal to the fetal circulation across the placenta (5). 

A small number of fetal cells cross the placental barrier and circulate in the mother s bloodstream. These can be isolated from a sample of the mother s blood using cell-sorting techniques, and DNA can be amplified by PCR for genetic diagnosis. Although still experimental, this technique offers the advantage that there is no risk of fetal loss as a result of the procedure. 

The rhesus D antigen occurs in 84% of all white individuals, who are therefore Rh-pos-itive. If an Rh-positive child is born to an Rh-negative mother, fetal erythrocytes can enter the mother s circulation during birth and lead to the formation of antibodies (IgG) against the D antigen. This initially has no acute effects on the mother or child. Complications only arise when there is a second pregnancy with an Rh-positive child, as maternal anti-D antibodies cross the placenta to the fetus even before birth and can trigger destruction of the child s Rh-positive erythrocytes [fetal erythroblastosis). 

In patients with impaired renal function, the serum half-life is prolonged. Pregnancy Category B. Aztreonam crosses the placenta and enters fetal circulation. Lactation Aztreonam is excreted in breast milk in concentrations that are less than 1% of maternal serum. Consider temporary discontinuation of nursing. 

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