Fetal and maternal estrogen concentrations throughout pregnancy in the sheep

1981 ◽  
Vol 59 (9) ◽  
pp. 970-978 ◽  
Author(s):  
John R. G. Challis ◽  
John E. Patrick
Keyword(s):  
Early Pregnancy ◽  
Time Course ◽  
Allantoic Fluid ◽  
Late Pregnancy ◽  
Fetal Lung ◽  
Lung Maturation ◽  
Similar Time ◽  
Fetal Plasma ◽  
Estrogen Production ◽  
Pregnant Sheep

Because of the possible importance of estrogens in events of early pregnancy, and in fetal lung maturation and parturition, we have measured unconjugated estrone (E1) and estradiol (E2) concentrations in amniotic fluid (AF) and allantoic fluid (ALF) from pregnant sheep, and have compared these values with estrogen concentrations in the fetal and maternal plasma. Samples were collected under acute conditions of general anaesthesia or from chronically catheterized animals during late pregnancy. E1 always exceeded E2 in AF and ALF. On days 100 to term, the concentrations of E1 sulphate in AF and ALF greatly exceeded those of E1 but decreased towards term. E1 was elevated in AF on day 50, decreased to day 100, and in chronic preparations increased significantly before birth, at the time of the prepartum rise in E1 in maternal and fetal plasma. E1 in ALF was higher than in AF on days 50 and 100, but no consistent pattern of E1 in ALF with gestation was established, due in part to substantial interanimal variation. Similar concentrations of E2 were found in AF and ALF. In AF, E2 rose significantly before birth, with a similar time course to the prepartum rise in E2 in maternal and fetal plasma. In early pregnancy, the ratio E1/E2 in umbilical cord blood was higher than in all other compartments. We conclude (1) there is evidence for estrogen production in early pregnancy (day 50), favouring E1; (2) E1 predominates over E2 in the fetal as well as maternal compartment, although its concentration in amniotic and allantoic fluid is substantially less than E1S; (3) parturition is preceeded by rising concentrations of E1 and E2 in AF as well as in maternal and fetal plasma; and (4) this increase probably reflects rising fetoplacental production and may indicate increasing estrogen availability to the fetal membranes, uterine and fetal tissues around the time of birth.

Atrial natriuretic factor in maternal and fetal sheep

1987 ◽  
Vol 252 (2) ◽  
pp. E279-E282 ◽  
Author(s):  
C. Y. Cheung ◽  
D. M. Gibbs ◽  
R. A. Brace
Keyword(s):  
Atrial Natriuretic Factor ◽  
Allantoic Fluid ◽  
Maternal Plasma ◽  
Fetal Kidney ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Natriuretic Factor ◽  
Pregnant Sheep ◽  
Fetal Urine ◽  
Atrial Natriuretic

To determine atrial natriuretic factor (ANF) concentrations in the circulation and body fluids of adult pregnant sheep and their fetuses, pregnant ewes were anesthetized with pentobarbital sodium, and the fetuses were exteriorized for sampling. ANF concentration, as measured by radioimmunoassay, was 47 +/- 6 (SE) pg/ml in maternal plasma, which was significantly higher than the 15 +/- 3 pg/ml in maternal urine. In the fetus, plasma ANF concentration was 265 +/- 49 pg/ml, 5.6 times that in maternal plasma. No umbilical arterial and venous difference in ANF concentration was observed. Fetal urine ANF concentration (13 +/- 2 pg/ml) was significantly lower than that in fetal plasma, and was similar to that measured in amniotic and allantoic fluid. In chronically catheterized maternal and fetal sheep, fetal plasma ANF was again 5.1 times that in maternal plasma, and these levels were not different from those measured in acutely anesthetized animals. These results demonstrate that immunoreactive ANF is present in the fetal circulation at levels higher than those found in the mother. The low concentration of ANF in fetal urine suggests that ANF is probably metabolized and/or reabsorbed by the fetal kidney.

Short-term fluctuations in the concentration of cortisol and progesterone in fetal plasma, maternal plasma, and amniotic and allantoic fluids from sheep during late pregnancy

1981 ◽  
Vol 59 (3) ◽  
pp. 261-267 ◽  
Author(s):  
J. R. G. Challis ◽  
J. E. Patrick ◽  
Jill Cross ◽  
J. Workewych ◽  
E. Manchester ◽  
...  
Keyword(s):  
Amniotic Fluid ◽  
Allantoic Fluid ◽  
Late Pregnancy ◽  
Maternal Plasma ◽  
Significant Rise ◽  
Short Term ◽  
Fetal Plasma ◽  
Two Fluids ◽  
Paired Samples ◽  
Steroid Profiles

Fluctuations in the concentrations of cortisol and progesterone in fetal plasma, maternal plasma, and amniotic and allantoic fluids were measured in samples taken at 10-min intervals over a 90-min period from three groups of sheep sampled at different times during late pregnancy. During the last 30 days of gestation there was a significant rise in the mean concentration of cortisol in fetal plasma and amniotic fluid and a significant correlation between the cortisol concentration in these two fluids. The concentration of cortisol in allantoic fluid exceeded that in amniotic fluid. The concentration of cortisol in fetal plasma varied in a pulsatile manner; however the coefficient of variation (CV) within animals was greater (36%) on days −11 to −20, relative to the day of parturition (day 0), than on days −21 to −30 or days −5 to 0 (15–19%). The CV values for cortisol in amniotic fluid and maternal plasma during the last 30 days of pregnancy were 20–50% and two to five times greater than the intraassay CV. The concentration of progesterone in amniotic fluid increased after day −20 but was not correlated with that in maternal plasma or fetal plasma. The concentrations of progesterone in paired samples of amniotic fluid and allantoic fluid were similar. The CV values for progesterone (18–34%) were similar in fetal and maternal plasma and amniotic fluid and did not change significantly during late pregnancy. Changes in the concentration of progesterone were unrelated to changes in cortisol. Interpretation of steroid profiles in fetal plasma and fluids through late pregnancy should take into account these short-term fluctuations in hormone concentrations.

scholarly journals Leptin receptor expression in fetal lung increases in late gestation in the baboon: a model for human pregnancy

Reproduction ◽  
2004 ◽  
Vol 127 (1) ◽  
pp. 87-94 ◽  
Author(s):  
M C Henson ◽  
K F Swan ◽  
D E Edwards ◽  
G W Hoyle ◽  
J Purcell ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Late Pregnancy ◽  
Fetal Lung ◽  
Transcript Abundance ◽  
Receptor Expression ◽  
Late Gestation ◽  
Receptor Protein ◽  
Lung Maturation ◽  
Primate Model ◽  
Human Pregnancy

Leptin produced by both adipose tissue and the placental trophoblast, has been proposed to regulate numerous aspects of human conceptus development. Although recent animal studies have suggested an additional role for the polypeptide in fetal lung maturation, no evidence has been reported in primates. Therefore, we employed the baboon (Papio sp.), a well-characterized primate model for human pregnancy, to determine the presence and ontogeny of leptin receptor in fetal lung with advancing gestation. Lungs were collected from fetal baboons, early in gestation (days 58–62, n = 4), at mid gestation (days 98–102, n = 4), and late in gestation (days 158–165, n = 4) (term 184 days). mRNA transcripts for leptin (LEP) and both long and short intracellular domain isoforms of the leptin receptor (LEP-RL and LEP-RS) were assessed by RT-PCR. leptin receptor protein was evaluated by immunoblotting and cell types expressing leptin receptor were identified in late pregnancy by immunohistochemistry. Fetal serum leptin concentrations, determined by RIA, remained relatively unchanged at 5.7 ± 1.1 ng/ml (mean ± s.e.m.) in mid pregnancy and 8.4 ± 3.0 ng/ml in late pregnancy (P > 0.05). Although leptin were detectable in fetal lung, no changes in transcript abundance were apparent with advancing gestation. However, transcripts for both LEP-RL and LEP-RS receptor isoforms increased several-fold (P < 0.05) in fetal lung between mid and late gestation, while leptin receptor protein was detectable only in late pregnancy. leptin receptor was localized in distal pulmonary epithelial cells, including type II pneumocytes. In conclusion, leptin is present in the fetal baboon and its receptor is enhanced during late gestation in cells responsible for the synthesis of pulmonary surfactant. Collectively, these and past findings may suggest a modulatory role for the polypeptide in pulmonary development and/or may identify leptin receptor as a physiological marker of primate fetal lung maturity.

INCREASE IN THE RESPONSE TO ADRENOCORTICOTROPHIN OF ISOLATED MATERNAL ADRENAL CELLS FROM SHEEP IN LATE PREGNANCY

1980 ◽  
Vol 86 (1) ◽  
pp. 93-100 ◽  
Author(s):  
J. A. GLICKMAN ◽  
J. E. PATRICK ◽  
J. R. G. CHALLIS
Keyword(s):  
Early Pregnancy ◽  
Post Partum ◽  
Late Pregnancy ◽  
Maximum Output ◽  
Maximal Concentration ◽  
Adrenal Cells ◽  
Melanocyte Stimulating Hormone ◽  
Pregnant Sheep ◽  
The Absolute

Adrenal cells were prepared from non-pregnant (anoestrous) sheep, from ewes at days 50, 100 and 130 of pregnancy and at term, and from animals at 1–5 days post partum. The ability of the cells to respond to adrenocorticotrophin (ACTH1–24), α-melanocyte-stimulating hormone (α-MSH), or combinations of these peptides has been examined in vitro. There was a progressive rise in the basal output of cortisol during pregnancy and in the absence of adrenocorticotrophin the cortisol output from adrenal cells of late pregnant and post-partum sheep was significantly greater than that from the non-pregnant animals. Adrenocorticotrophin increased cortisol output by adrenal cells at all times tested. In anoestrous sheep the amount of ACTH required to produce half the maximum output of steroid (ED50) was 8 pg/ml. The ED50 increased in early pregnancy to 112 pg/ml and then fell to < 5 pg/ml between day 100 and term. At term both the stimulation ratio and the absolute increment in cortisol output elicited by a maximal concentration of ACTH were greater than at any other time tested in pregnant or non-pregnant sheep. Cortisol output during pregnancy was not increased by α-MSH, although at term the stimulatory effect of ACTH1–24 was partially antagonized by α-MSH. These results suggest that there may be an increase in the responsiveness of the maternal adrenal during pregnancy, although the factor(s) responsible remains unknown.

scholarly journals Fetal Lung Maturation in Estrogen-Deprived Baboons

2003 ◽  
Vol 88 (1) ◽  
pp. 471-477 ◽  
Author(s):  
Gerald J. Pepe ◽  
Philip L. Ballard ◽  
Eugene D. Albrecht
Keyword(s):  
Fetal Lung ◽  
Serum Cortisol ◽  
Hydroxysteroid Dehydrogenase ◽  
Placental Development ◽  
Lung Maturation ◽  
Estrogen Production ◽  
Dehydrogenase Enzyme ◽  
Cortisol Levels ◽  
Fetal Lungs ◽  
Cgs 20267

We have previously shown that estrogen plays a central integrative role in regulating key aspects of fetal-placental development and that inhibition of estrogen production during the second half of baboon pregnancy suppressed fetal adrenal function. Because maturation of the fetal lung is dependent on cortisol of fetal adrenal origin, the current study determined whether lung development and expression of surfactant proteins (SPs) A and B were altered at term in estrogen-deprived baboons. Fetal lungs were obtained on d 100, 165, and 175 of gestation (term = d 184) from untreated baboons and on d 165 from animals treated daily during the second half of pregnancy either with the aromatase inhibitor CGS 20267 alone or with CGS 20267 and estradiol benzoate. Umbilical venous estradiol levels were suppressed by more than 95% by CGS 20267 and elevated by CGS 20267 and estrogen. Although umbilical serum cortisol levels were also suppressed by 35% by CGS 20267, cortisol levels in the fetal lung of estrogen-suppressed baboons were similar to values in untreated animals. Immunocytochemistry demonstrated that CGS 20267 treatment did not alter fetal lung expression of the 11β-hydroxysteroid dehydrogenase enzyme-1 enzyme catalyzing reduction of cortisone to cortisol. However, immunocytochemical expression of the 11β-hydroxysteroid dehydrogenase enzyme-2 catalyzing oxidation of cortisol to cortisone appeared lower in lungs of estrogen-deprived fetuses and restored to normal by CGS 20267 and estrogen. SP-A levels in fetal lungs of untreated baboons were increased 16- to 20-fold between d 100 and d 165–175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Similarly, SP-B levels in fetal lungs of untreated baboons were increased 10-fold between d 100 and d 165–175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Moreover, in estrogen-suppressed baboons, as in untreated animals, the fetal lung continued to grow and exhibited normal alveolarization on histology. We conclude that development of the primate fetal lung can occur in utero in baboons in which fetal serum cortisol levels have been suppressed by the relative absence of estrogen perhaps because of the ability of the lung to coordinate local production of cortisol.

Glucocorticoid regulation of surfactant components in immature lambs

1997 ◽  
Vol 273 (5) ◽  
pp. L1048-L1057 ◽  
Author(s):  
Philip L. Ballard ◽  
Yue Ning ◽  
Daniel Polk ◽  
Machiko Ikegami ◽  
Alan H. Jobe
Keyword(s):  
Lung Function ◽  
Fold Increase ◽  
Fetal Lung ◽  
Lavage Fluid ◽  
Efficiency Index ◽  
Lung Maturation ◽  
Glucocorticoid Treatment ◽  
Similar Dose ◽  
Pregnant Sheep ◽  
Fluid Levels

To assess effects of dose and duration of glucocorticoid exposure on maturation of the fetal lung, we administered single or multiple doses of betamethasone (0.5 mg/kg im) to pregnant sheep for 2 or 21 days before preterm delivery at 125 days of gestation. Lung function (compliance, lung volume at 40 cmH2O pressure, and ventilatory efficiency index) was increased after two to four weekly doses of glucocorticoid (2.5- to 4-fold increase) and after 48 h of exposure (1.4- to 2.3-fold). Total protein of lavage fluid decreased similarly with three doses, four doses, and 48 h of treatment. In lambs with long-term exposure to betamethasone, there was a similar, dose-dependent increase in concentrations of saturated phosphatidylcholine and surfactant proteins A (SP-A) and B (SP-B) (maximal 2- to 3-fold in tissue and 10- to 15-fold in lavage fluid). Levels of SP-A and SP-B were closely correlated in lavage fluid. In animals treated for 48 h, only tissue SP-B was increased (2.7-fold). We conclude that 48 h of glucocorticoid treatment improves lung function in the premature lamb without a detectable increase in lavage surfactant components and that longer exposure to antenatal glucocorticoid increases surfactant lipid and proteins in a coordinated fashion. The enhanced response with repetitive dosing indicates that the process of glucocorticoid-induced lung maturation is either reversible and/or gestational age dependent.

scholarly journals Pre-implantation exogenous progesterone and pregnancy in sheep. II. Effects on fetal-placental development and nutrient transporters in late pregnancy

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Katherine M. Halloran ◽  
Emily C. Hoskins ◽  
Claire Stenhouse ◽  
Robyn M. Moses ◽  
Kathrin A. Dunlap ◽  
...  
Keyword(s):  
Amniotic Fluid ◽  
Corn Oil ◽  
Allantoic Fluid ◽  
Late Pregnancy ◽  
Maternal Plasma ◽  
Nutrient Transporters ◽  
Placental Development ◽  
Blastocyst Development ◽  
Fetal Plasma ◽  
Exogenous Progesterone

Abstract Background Administration of progesterone (P4) to ewes during the first 9 to 12 days of pregnancy accelerates blastocyst development by day 12 of pregnancy, likely due to P4-induced up-regulation of key genes in uterine epithelia responsible for secretion and transport of components of histotroph into the uterine lumen. This study determined if acceleration of blastocyst development induced by exogenous P4 during the pre-implantation period affects fetal-placental development on day 125 of pregnancy. Suffolk ewes (n = 35) were mated to fertile rams and assigned randomly to receive daily intramuscular injections of either corn oil vehicle (CO, n = 18) or 25 mg progesterone in CO (P4, n = 17) for the first 8 days of pregnancy. All ewes were hysterectomized on day 125 of pregnancy and: 1) fetal and placental weights and measurements were recorded; 2) endometrial and placental tissues were analyzed for the expression of candidate mRNAs involved in nutrient transport and arginine metabolism; and 3) maternal plasma, fetal plasma, allantoic fluid, and amniotic fluid were analyzed for amino acids, agmatine, polyamines, glucose, and fructose. Results Treatment of ewes with exogenous P4 did not alter fetal or placental growth, but increased amounts of aspartate and arginine in allantoic fluid and amniotic fluid, respectively. Ewes that received exogenous P4 had greater expression of mRNAs for SLC7A1, SLC7A2, SLC2A1, AGMAT, and ODC1 in endometria, as well as SLC1A4, SLC2A5, SLC2A8 and ODC1 in placentomes. In addition, AZIN2 protein was immunolocalized to uterine luminal and glandular epithelia in P4-treated ewes, whereas AZIN2 localized only to uterine luminal epithelia in CO-treated ewes. Conclusions This study revealed that exogenous P4 administered in early pregnancy influenced expression of selected genes for nutrient transporters and the expression of a protein involved in polyamine synthesis on day 125 of pregnancy, suggesting a ‘programming’ effect of P4 on gene expression that affected the composition of nutrients in fetal-placental fluids.

Thyrotrophin-releasing hormone (TRH) and lung maturation

1995 ◽  
Vol 7 (3) ◽  
pp. 443 ◽  
Author(s):  
GC Liggins
Keyword(s):  
Fetal Lung ◽  
Lung Maturation ◽  
Rabbit Lung ◽  
Glucocorticoid Treatment ◽  
Fetal Sheep ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Plasma

Clinical trials of thyrotrophin-releasing hormone (TRH) in conjunction with antepartum glucocorticoid treatment in the prevention of respiratory distress syndrome is based on experimental evidence that fetal lung maturation is accelerated by exposure to raised concentrations of triiodothyronine (T3) in fetal plasma. Studies of fetal rat and rabbit lung in vitro show an inconsistent increase in surfactant synthesis in response to T3 and potentiation of the response to corticosteroid. Experiments with fetal rodents in vivo are difficult to interpret because of confounding effects of the procedures and the responses to T3 are variable. In fetal sheep, very high concentrations of T3 are without effect on lung maturation. These observations suggest that the action of TRH on the lung may be mediated at least in part by one of the numerous, non-hormonal pathways known to be stimulated by TRH, particularly the autonomic nervous system. Experiments in rats and sheep lend support to this possibility. It is concluded that available evidence is inadequate to determine the mechanism of action of TRH.

Postnatal growth rate and gonadal development in circadian tau mutant hamsters reared in constant dim red light

Reproduction ◽  
2000 ◽  
pp. 327-330 ◽  
Author(s):  
RJ Lucas ◽  
JA Stirland ◽  
YN Mohammad ◽  
AS Loudon
Keyword(s):  
Time Course ◽  
Red Light ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Gonadal Development ◽  
Testicular Development ◽  
Wild Type ◽  
Similar Time ◽  
Syrian Hamsters ◽  
Body Weights

The role of the circadian clock in the reproductive development of Syrian hamsters (Mesocricetus auratus was examined in wild type and circadian tau mutant hamsters reared from birth to 26 weeks of age under constant dim red light. Testis diameter and body weights were determined at weekly intervals in male hamsters from 4 weeks of age. In both genotypes, testicular development, subsequent regression and recrudescence exhibited a similar time course. The age at which animals displayed reproductive photosensitivity, as exhibited by testicular regression, was unrelated to circadian genotype (mean +/- SEM: 54 +/- 3 days for wild type and 59 +/- 5 days for tau mutants). In contrast, our studies revealed a significant impact of the mutation on somatic growth, such that tau mutants weighed 18% less than wild types at the end of the experiment. Our study reveals that the juvenile onset of reproductive photoperiodism in Syrian hamsters is not timed by the circadian system.

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