Placental Diffusion Research Articles

Maternal and fetal plasmsa levels of free corticosteroids during normal delivery.

An increase in the concentration of free corticosteroids, especially of cortisol, with increasing gestational age in the maternal plasma [4, 5, 6, 9, 11] and in the umbilical vessels [4, 11, 18, 19] as well as in the maternal plasma during delivery [3, 4, 5, 13] is well known. The influence of placental diffusion and of the fetal adrenal cortex have been studied in detail [l, 2, 11, 12, 14]. While some authors [4, 8] have demonstrated a cofrelation between fetal plasma corticosteroid values and maternal plasma concentrations, other investigators have denied this correlation [5, 7]. Differences in the methodology and a varying selection of the material for investigation have lead to great discrepancies in the results. This paper will deal with the changes of free corticosteroids in fetal and maternal plasma during normal vaginal deliveries. Total corticosteroids were determined which after plasma extraction are bound to corticosteroid bindingglobulin (CBG = transcortin).

Umbilical blood flow, cardiac output, and organ blood flow in the immature baboon fetus

Seven immaturebbaboon fetuses were studied in an acute surgical protocol at 116 to 124 days' gestation (term = 184). Mean umbilical blood flow was 121 ± 29 ml. per minute per kilogram, mean cardiac output was 219 ± 30 ml. per minute per kilogram, and mean placental diffusion clearance of antipyrine was 75 ± 17 ml. per minute per kilogram. These data were similar to those previously obtained in mature baboon fetuses. Blood flow to organs drained by the superior vena cava was 50 per cent less in the immature compared to mature fetuses. Blood flow to the paleoencephalon as a percentage of cardiac output was significantly higher in the mature fetuses, a difference not completely explained by the increase in organ weight. One immature fetus was severely acidotic and showed the biochemical and circulatory changes associated with asphyxia.

Umbilical blood flow, fetal oxygen consumption and placental diffusion clearance of antipyrine in the baboon

Umbilical blood flow in the baboon fetus near term was measured using the antipyrine diffusion method. The mean umbilical blood flow for seven fetuses of five mothers was 104.2 ± 32.2 ml/min/kg. The mean fetal oxygen consumption was 5.7 ± 2.0 ml/min/kg. The mean placental diffusion clearance of antipyrine was 54.5 ± 15 ml/min/kg. The baboon fetuses had significantly lower umbilical blood flows than rhesus monkey fetuses (Behrman, Peterson and deLannoy, 1969) under the same conditions of an acute experimental protocol using general anesthesia for the mothers; oxygen consumption and antipyrine diffusion clearances were similar for both species. The lack of a significant difference in oxygen consumption despite a lower umbilical blood flow in the baboon fetuses may be related to the difference in position of the oxygen-hemoglobin dissociation curve and or the greater extraction of oxygen by the baboon placenta and fetus. The antipyrine diffusion clearance data were consistent with the oxygen consumption data and suggest greater efficiency of placental transfer of antipyrine as well as oxygen across the baboon placenta compared to the rhesus monkey placenta.

Control of Glucose Metabolism in the Human Fetus and Newborn Infant

As normal human gestation progresses, the secretion of a hormone that is unique to the trophoblast—human placental lactogen—begins early in pregnancy and increases toward term, and the concentration of this hormone in maternal plasma rises progressively. In association with the high plasma levels sustained at term, resistance to the normal enhancement of glucose uptake by insulin develops in pregnant women. Thus, the rate of glucose metabolism by the fasting pregnant woman declines, and the decreased maternal uptake of glucose helps to preserve the fasting plasma level of glucose even though it diffuses continuously to the fetus. Although insulin resistance can be demonstrated in late pregnancy, normal glucose tolerance is maintained; after the ingestion of glucose, the plasma insulin response is enhanced. Thus, at the end of gestation, a hormonal factor other than placental lactogen causes an excessive insulin response to glucose stimuli. Throughout pregnancy, there is a net placental diffusion of glucose from the mother to the fetus as long as the mother remains either normoglycemic or hyperglycemic; but the protein hormones which could participate in the control of fetal glucose metabolism are transferred poorly.