Distribution of relaxin between human maternal and fetal circulations and amniotic fluid

1992 ◽  
Vol 134 (2) ◽  
pp. 313-317 ◽  
Author(s):  
M. R. Johnson ◽  
A. Abbas ◽  
K. H. Nicolaides ◽  
S. L. Lightman

ABSTRACT Relaxin was measured in maternal blood and amniotic fluid samples at 9–40 weeks and in fetal blood samples at 19–41 weeks of pregnancy. In amniotic fluid, concentrations of relaxin rose from 58 ng/1 (geometric mean) at 10 weeks to 142 ng/l at 14 weeks and declined subsequently to 55 ng/l at 22 weeks. In maternal blood, mean relaxin concentrations were ten times greater than in amniotic fluid, and concentrations decreased with gestation. Since there was no significant association between the relaxin concentrations in the two compartments, relaxin in the amniotic fluid may be derived from the decidualized endometrium rather than the maternal circulation, alternatively its metabolism may be different in the two compartments. The absence of detectable concentrations of relaxin in any of the fetal blood samples demonstrates that there is no significant placental transfer or fetal synthesis of this peptide. Journal of Endocrinology (1992) 134, 313–317

1996 ◽  
Vol 30 (11) ◽  
pp. 1249-1251 ◽  
Author(s):  
Maria L Santeiro ◽  
Carine Stromquist ◽  
Lance Wyble

OBJECTIVE: To report phenoxybenzamine placental transfer in the treatment of maternal hypertension secondary to pheochromocytoma. CASE SUMMARY: A 22-year-old woman diagnosed with pheochromocytoma was medically managed at 33 weeks gestation with oral phenoxybenzamine and labetalol until delivery 26 days later. To determine phenoxybenzamine placental passage, at the time of cesarean section simultaneous samples were obtained from the cord blood, maternal blood, and amniotic fluid. Additional blood samples were obtained from the newborn at 32 and 80 hours of life. Mean concentrations of phenoxybenzamine from cord and maternal plasma and in amniotic fluid were 103.3,66, and 79.3 ng/mL, respectively; the newborn's plasma concentration at 32 hours of life was 22.3 ng/mL. At the time of delivery, the 2475-g male infant exhibited perinatal depression; mild transient hypotension was also noted for the first few days of life. DISCUSSION: The fetal—maternal plasma accumulation ratio of 1.6:1 indicates that at this gestational age after 26 days of therapy, the placental transfer of phenoxybenzamine occurs and is accompanied by accumulation in the fetal blood. CONCLUSIONS: Because of the placental transfer of phenoxybenzamine, mild perinatal depression and transient hypotension may occur in newborns of mothers receiving this medication. These newborns must be closely monitored during the first few days of life for respiratory depression and hypotension.


1981 ◽  
Vol 50 (5) ◽  
pp. 999-1005 ◽  
Author(s):  
J. Qvist ◽  
R. E. Weber ◽  
W. M. Zapol

Oxygen equilibria of whole blood and hemoglobins from adult and fetal Weddell seals are reported. The maternal blood shows a lower O2 affinity than the fetal blood (halfsaturation O2 tension P50 = 26.9 +/- 1.18 and 21.4 +/- 1.25 Torr, respectively, at 37 degrees C and pH 7.4), and a greater Bohr effect (delta log P50/delta pH = -0.49 and -0.31, respectively, at pH 7.4-6.8), correlated with higher red cell 2,3-diphosphoglycerate (2,3-diphosphoglycerate (2,3-DPG) concentrations (6.45 +/- 0.81 mmol.1-1, compared to 2.65 +/- 0-42 mmol.1-1 in the fetus). Both the maternal and fetal erythrocytes contain two major and two minor hemoglobin components occurring in the same ratio and the 2,3-DPG-free whole hemolysates, as well as the isolated major components from each stage, show the same oxygenation properties, ascribing the whole-blood differences to the higher adult DPG levels. A 2,3-DPG effect also appears to account for the disparity in the Bohr effects, which will favor unloading of O2 from the maternal circulation during diving as maternal and fetal blood pH decrease in parallel.


1976 ◽  
Vol 230 (2) ◽  
pp. 357-361 ◽  
Author(s):  
VC Char ◽  
RK Creasy

Fetal acetate metabolsim was studied in chronically catheterized fetal lambs of 110-141 days' gestation. Acetate concentration was measured enzymatically in whole blood drawn simultaneously from maternal and fetal pre- and postplacental vessels. The oxygen content of the fetal blood samples was also measured. Fetal umbilical venous acetate concentration was found to be proportional to the maternal arterial acetate concentration and had a mean value of 0.366 mM. Fetal blood acetate increased significantly, by a mean of 0.081 mM, during circulation through the placenta. This increase was proportional to both the maternal acetate concentration and the concentration gradient of acetate across the placenta. The mean maternal arterial acetate concentration was 1.153 mM. Maternal blood lost significant amounts of acetate, 0.112 mM, during circulation through the uterus and appeared to be the source of the acetate being gained by the fetus. It is estimated that a total of 23 mmol of acetate/kg of fetal weight is being taken up by the fetus each day, providing it with 0.560 g of carbon/kg. Comparisons of acetate uptake with fetal oxygen uptake indicate 10% of the daily fetal oxygen consumption would be required to completely oxidize the acetate being gained by the fetus.


1986 ◽  
Vol 64 (8) ◽  
pp. 1060-1067 ◽  
Author(s):  
David W. Clarke ◽  
Nancy A. E. Steenaart ◽  
Christopher J. Slack ◽  
James F. Brien

The pharmacokinetics of ethanol and its metabolite, acetaldehyde, were determined in the third-trimester pregnant guinea pig (56–59 days gestation) for oral intubation of four doses of 1 g ethanol/kg maternal body weight, administered at 1-h intervals. Animals (n = 4–7) were sacrificed at each of selected times during the 26-h study. Ethanol and acetaldehyde concentrations were determined by headspace gas-liquid chromatography. The maternal and fetal blood ethanol concentration–time curves were virtually superimposable, which indicated unimpeded bidirectional placental transfer of ethanol in the matemal–fetal unit. The blood and brain ethanol concentrations were similar in each of the maternal and fetal compartments during the study, which indicated rapid equilibrium distribution of ethanol. There was accumulation of ethanol in the amniotic fluid resulting in higher ethanol concentration compared with maternal and fetal blood during the elimination phase, which indicated that the amniotic fluid may serve as a reservoir for ethanol in utero. Acetaldehyde was measurable in all the biological fluids and tissues at concentrations that were at least 1000-fold less than the respective ethanol concentrations and were variable. There was ethanol-induced fetolethality that was delayed and variable among animals, and was 55% at 23 h. At this time interval, the ethanol concentrations in maternal blood and brain, fetal brain, and amniotic fluid were 35- to 53-fold greater and the acetaldehyde concentrations in maternal blood and fetal brain were four- to five-fold higher in the animals with dead fetuses compared with the guinea pigs with live litters. These data indicated that decreased ethanol elimination from the maternal–fetal unit was related temporally to the fetolethality.


Reproduction ◽  
2002 ◽  
pp. 259-265 ◽  
Author(s):  
◽  
Y Xia ◽  
T O'Shea ◽  
S Hayward ◽  
AE O'Connor ◽  
...  

The aim of this study was to investigate the changes in follistatin, an activin binding protein, during the oestrous cycle, gestation and parturition in ewes using a radioimmunoassay for total follistatin, which uses dissociating reagents to remove the interference of activin. Follistatin concentrations remained unchanged (2.7 +/- 0.2 ng ml(-1)) during the oestrous cycle and decreased as pregnancy progressed. Follistatin concentrations in allantoic fluid also decreased during gestation, whereas in amniotic fluid follistatin concentrations reached a peak at day 75 of gestation (9.8 ng ml(-1)) and had decreased to 4.4 ng ml(-1) at day 140. Follistatin concentrations in fetal blood (7.0 +/- 0.5 ng ml(-1)) did not change from day 50 to day 140 of gestation but were significantly higher than in matched maternal samples (3.1 +/- 0.3 ng ml(-1)). Circulating follistatin in ewes was significantly increased on the day of parturition (5.6 +/- 0.6 ng ml(-1)) compared with the days before parturition (2.7 +/- 0.4 ng ml(-1)), but had decreased by day 2 after birth. Blood samples from newborn lambs showed that plasma follistatin concentration (13.4 +/- 2.3 ng ml(-1)) was significantly higher than that of the mothers and remained high for at least 7 days after birth. These data support previous studies of the human menstrual cycle indicating that follistatin is not an endocrine signal from the ovary; however, in contrast to human pregnancies, follistatin concentrations in sheep decreased and become high only after or during parturition. This difference observed between species may reflect different physiological effects of follistatin or may be the result of measurement of different isoforms.


1980 ◽  
Vol 86 (2) ◽  
pp. 305-310 ◽  
Author(s):  
E. M. WINTOUR ◽  
J. P. COGHLAN ◽  
K. J. HARDY ◽  
B. E. LINGWOOD ◽  
M. RAYNER ◽  
...  

To determine the percentage of the maternal secretion of aldosterone which crosses the placenta the blood clearance rate (BCR) of aldosterone was measured in pregnant sheep and in chronically cannulated fetuses by the constant infusion of [3H]aldosterone alternately into the maternal and fetal compartments. When equilibrium had been reached the concentration of [3H]aldosterone was measured in both maternal and fetal compartments. Aldosterone BCR in eight pregnant ewes was 98 ± 5 (s.e.m.) litres/h which was not significantly different from that of ten non-pregnant ewes at 95 ± 5 litres/h. The BCR of aldosterone in seven fetuses was 24 ± 2 litres/h. A small percentage (4·4 ± 0·3; n = 7) of the maternal production rate was transferred to the fetus, whilst 29 ± 4% (n = 8) of the fetal production rate was transferred to the maternal compartment. When aldosterone was measured in maternal and fetal blood samples collected simultaneously from sodium-replete sheep more than 80% of the aldosterone in fetal blood was of fetal origin if the actual fetal concentration of aldosterone was greater than 1·5 ng/dl.


1969 ◽  
Vol 105 (7) ◽  
pp. 1069-1071 ◽  
Author(s):  
Gerald Carrier ◽  
Arthur S. Hume ◽  
Ben H. Douglas ◽  
Winfred L. Wiser

Sign in / Sign up

Export Citation Format

Share Document