Distribution between Protein-Bound and Free Forms of Plasma Cortisol in the Gilt and Fetal Pig Near Term

Neonatology ◽  
1997 ◽  
Vol 72 (3) ◽  
pp. 192-200 ◽  
Author(s):  
H.G. Kattesh ◽  
G.A. Baumbach ◽  
B.B. Gillespie ◽  
J.F. Schneider ◽  
J.T. Murai
Keyword(s):  
2002 ◽  
Vol 173 (1) ◽  
pp. 143-150 ◽  
Author(s):  
AJ Forhead ◽  
AL Fowden

In the sheep fetus, pulmonary and renal concentrations of angiotensin-converting enzyme (ACE) increase towards term in parallel with the prepartum surges in plasma cortisol and tri-iodothyronine (T(3)). The ontogenic change in pulmonary ACE has been shown to be induced, at least in part, by cortisol but the role of the thyroid hormones is unknown. Therefore, this study investigated the effects of thyroid hormones on tissue ACE concentration in fetal sheep during late gestation. Pulmonary and renal ACE concentrations were measured in sheep fetuses after experimental manipulation of thyroid hormone status by fetal thyroidectomy and exogenous hormone infusion. In intact fetuses, pulmonary and renal ACE concentrations increased between 127-132 and 142-145 days of gestation (term 145 +/- 2 days), coincident with the prepartum rises in plasma cortisol and T(3). The ontogenic increment in pulmonary ACE concentration was abolished when the prepartum surge in T(3), but not cortisol, was prevented by fetal thyroidectomy. At 143-145 days, ACE concentration in the lungs and kidneys of the thyroidectomised fetuses were both lower than those in the intact fetuses. In intact fetuses at 127-132 days, pulmonary ACE was upregulated by intravenous infusions of either cortisol (2-3 mg/kg per day) or T(3) (8-12 microg/kg per day) for 5 days. Renal ACE was unaffected by cortisol or T(3) infusion. Therefore, thyroid hormones have an important role in the developmental control of pulmonary and renal ACE concentration in the sheep fetus towards term. In addition, the prepartum rise in plasma T(3) appears to mediate, in part, the maturational effect of cortisol on pulmonary ACE concentration.


1968 ◽  
Vol 40 (1) ◽  
pp. 37-47 ◽  
Author(s):  
J. Y. F. PATERSON ◽  
F. A. HARRISON

SUMMARY Tritium-labelled cortisol was administered to sheep by intravenous infusion at constant rate for up to 4 hr. When the infusion was stopped, [3H] cortisol disappeared rapidly from plasma and its concentration could be described by a double exponential function. There was good agreement between the results from 50 experiments on 11 sheep. In pregnant ewes, there was no noticeable difference in the rate of disappearance of [3H]cortisol from plasma until about 2 weeks before lambing, when the rate became more rapid. These data were interpreted in terms of a two-compartment model of cortisol distribution. The central compartment contains about 42 μg. cortisol and may be identical with the cortisol contained in whole blood volume. The outer compartment contains about 130 μg. cortisol; less than half of this compartment may be in intercellular fluids, partly bound to protein, and the remainder in intracellular fluids. In pregnant ewes near term there is a decrease in plasma cortisol concentration which appears to result from expansion of plasma volume. The decrease in unbound cortisol concentration probably results in a decrease in the size of the outer compartment of cortisol. This may contribute to the observed increase in the rate of disappearance of [3H] cortisol from plasma, but this change may also coincide with the initiation of secretion of cortisol by the foetus, at about 1 or 2 μg./min.


2004 ◽  
Vol 52 (4) ◽  
pp. 379-387 ◽  
Author(s):  
Ewa Brzezińska-Ślebodzińska ◽  
A. B. Ślebodziński

The concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3; rT3) in thyroid gland tissue and serum of the fetal pig (n = 68) from day 39 to 113 of gestation were measured. Tracer quantities of iodothyronines, displaying the onset of thyroid hormone activity, were found in the thyroid tissue on day 39, i.e. before the appearance of a measurable quantity of iodothyronines in the serum. The T4 and T3 thyroidal content showed the first rise between days 56 and 76. Then, T3 was increasing sharply from day 92 till birth, while T4 content was decreasing from about day 76 to a low value between day 92 and 105, and then showing an increase shortly before birth. The rT3 content was the highest on day 39 and then it was steadily decreasing to reach a nadir on about day 76. Measurable amounts of thyroid hormones (TH) in the serum were observed not earlier than on day 46 of gestation. Near birth, the tissues of the pig fetus are in a milieu characterised by the highest blood TH concentrations. The serum to thyroid concentration ratio for rT3 and T4 was generally below 1.0 until the last trimester of gestation, when it was over 5.0 for rT3 and over 4.0 for T4. By contrast, the T3 serum to thyroid ratio was below 0.5 throughout the gestation. The results show that the fetal pig thyroid displays a low rT3 and T4 content, but the marked T3 elevation observed near term supports the view that a high production and secretion of T3 near term may be a critical factor for normal postnatal adaptation to extrauterine cooling in the pig.


1972 ◽  
Vol 50 (5) ◽  
pp. 407-410 ◽  
Author(s):  
R. G. Brown ◽  
W. H. Harris ◽  
J. N. Cummings

The effects of birth on tissue and serum ascorbate levels as well as the influence of maternal hypoxia on fetal tissue and serum ascorbate levels were investigated. Serum and adrenal ascorbate levels in neonatal swine were drastically decreased when compared with near-term (112-day-old) fetal swine. Kidney, cardiac, and muscle ascorbate levels also were found to be decreased on birth although liver levels in the newborn rose significantly above fetal levels. Hypoxic stress produced by decreasing the oxygen concentration in the maternal gas supply produced effects in 112-day-old fetal pigs which were similar to those noted for birth. An hypothesis was presented to explain the observation in which it was suggested that ascorbate may have a key role in the mechanism by which the fetal pig successfully coped with the stress of birth.


Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5988-5994 ◽  
Author(s):  
Alison J. Forhead ◽  
Katrina Curtis ◽  
Ellen Kaptein ◽  
Theo J. Visser ◽  
Abigail L. Fowden

Preterm infants have low serum T4 and T3 levels, which may partly explain the immaturity of their tissues. Deiodinase enzymes are important in determining the bioavailability of thyroid hormones: deiodinases D1 and D2 convert T4 to T3, whereas deiodinase D3 inactivates T3 and produces rT3 from T4. In human and ovine fetuses, plasma T3 rises near term in association with the prepartum cortisol surge. This study investigated the developmental effects of cortisol and T3 on tissue deiodinases and plasma thyroid hormones in fetal sheep during late gestation. Plasma cortisol and T3 concentrations in utero were manipulated by exogenous hormone infusion and fetal adrenalectomy. Between 130 and 144 d of gestation (term 145 ± 2 d), maturational increments in plasma cortisol and T3, and D1 (hepatic, renal, perirenal adipose tissue) and D3 (cerebral), and decrements in renal and placental D3 activities were abolished by fetal adrenalectomy. Between 125 and 130 d, iv cortisol infusion raised hepatic, renal, and perirenal adipose tissue D1 and reduced renal and placental D3 activities. Infusion with T3 alone increased hepatic D1 and decreased renal D3 activities. Therefore, in the sheep fetus, the prepartum cortisol surge induces tissue-specific changes in deiodinase activity that, by promoting production and suppressing clearance of T3, may be responsible for the rise in plasma T3 concentration near term. Some of the maturational effects of cortisol on deiodinase activity may be mediated by T3.


1994 ◽  
Vol 140 (3) ◽  
pp. 425-430 ◽  
Author(s):  
E T M Berdusco ◽  
W K Milne ◽  
J R G Challis

Abstract Synthetic glucocorticoids stimulate the production of corticosteroid-binding globulin (CBG) by the liver of the sheep fetus near term (day 145). We have examined whether physiological changes in plasma cortisol alter plasma CBG concentrations, patterns of glycosylation and the amount of hepatic CBG mRNA at earlier times during pregnancy (day 100), prior to the activation of fetal hypothalamic-pituitary-adrenal function. Cortisol was infused into chronically catheterized sheep fetuses in amounts that raised the plasma cortisol concentration by about 15 nmol/l. This treatment resulted in a significant increase in the plasma corticosteroid-binding capacity and in the amount of CBG mRNA in the fetal liver, but did not alter the proportion of CBG retained using Concanavalin A chromatography. We conclude that the CBG gene in the liver of fetal sheep responds to physiological changes in plasma concentration of cortisol and we speculate that the rise in plasma CBG concentration is important in diminishing the negative feedback effect of circulating cortisol on the fetal pituitary and hypothalamus. Journal of Endocrinology (1994) 140, 425–430


Endocrinology ◽  
2002 ◽  
Vol 143 (4) ◽  
pp. 1166-1173 ◽  
Author(s):  
A. J. Forhead ◽  
L. Thomas ◽  
J. Crabtree ◽  
N. Hoggard ◽  
D. S. Gardner ◽  
...  

Abstract The ontogeny and developmental control of plasma leptin concentration in the fetus are poorly understood. The present study investigated plasma leptin concentration in chronically catheterized sheep fetuses near term, and in neonatal and adult sheep. The effect of glucocorticoids on plasma leptin in utero was examined by fetal adrenalectomy and exogenous cortisol or dexamethasone infusion. In intact, untreated fetuses studied between 130 and 140 d (term, 145 ± 2 d), plasma leptin concentration increased in association with the prepartum cortisol surge. Positive relationships were observed between plasma leptin in utero and both gestational age and plasma cortisol. Plasma leptin was also inversely correlated with fetal paO2. The ontogenic rise in plasma leptin was abolished by fetal adrenalectomy. In intact fetuses at 123–127 d, plasma leptin was increased by infusions of cortisol (3–5 mg kg−1d−1, +127 ± 21%) for 5 d and dexamethasone (45–60 μg kg−1d−1, +268 ± 61%) for 2 d. However, the cortisol-induced rise in plasma leptin was transient; by the fifth day of infusion, plasma leptin was restored to within the baseline range. These findings show that, in the sheep fetus, an intact adrenal gland is required for the normal ontogenic rise in plasma leptin near term. Furthermore, fetal treatment with exogenous and endogenous glucocorticoids increases circulating leptin concentration in utero.


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