scholarly journals The effects of psychosomatic stress at the end of pregnancy on maternal and fetal plasma cortisol levels and liver glycogen in guinea-pigs

1984 ◽  
Vol 24 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Pascale DAUPRAT ◽  
G. MONIN ◽  
M. DALLE ◽  
P. DELOST
1976 ◽  
Vol 70 (2) ◽  
pp. 207-214 ◽  
Author(s):  
M. DALLE ◽  
P. DELOST

SUMMARY Concentrations of cortisol, corticosterone and cortisone in the plasma and adrenal glands, liver glycogen and plasma glucose of foetal, newborn and mother guinea-pigs were estimated during the last 6 days of pregnancy and throughout the first 24 h post partum. At the same time progesterone was measured in the plasma of the mother. During the prepartum rise in foetal plasma cortisol levels and liver glycogen, no significant change in the foetal adrenal cortisol content was observed. The plasma and adrenal cortisol concentrations of the mother were much higher than those observed in the foetus and increased significantly before parturition. In the mother as in the foetus, cortisone and corticosterone represent only a small percentage of corticosteroids compared with cortisol. These results indicate that the autonomous capacity of foetal adrenals, inhibited by maternal secretions before term, appears suddenly at birth.


2001 ◽  
Vol 280 (5) ◽  
pp. E729-E739 ◽  
Author(s):  
Li Liu ◽  
Antai Li ◽  
Stephen G. Matthews

Pregnant guinea pigs were treated with dexamethasone (1 mg/kg) or vehicle on days 40–41, days 50–51, and days 60–61 of gestation. Adult offspring were split into two groups. Group 1 guinea pigs were catheterized, and the hypothalamo-pituitary-adrenal (HPA) axis was tested in basal and activated states. Group 2 guinea pigs were euthanized with no further manipulation. In male offspring, prenatal dexamethasone exposure resulted in a significant reduction in brain-to-body weight ratio. Dexamethasone-exposed male offspring exhibited reduced basal and activated plasma cortisol levels, which was associated with elevated hippocampal mineralocorticoid receptor (MR) mRNA and increased plasma testosterone. In females exposed to glucocorticoids in utero, basal and stimulated plasma cortisol levels were higher in the follicular and early luteal phases of the cycle, but this effect was reversed in the late luteal phase, indicating a significant interaction of sex steroids. In female offspring (at estrus), glucocorticoid receptor mRNA levels were lower in the paraventricular nucleus and pars distalis but higher in the hippocampus in animals exposed to dexamethasone in utero. Hippocampal MR mRNA levels were significantly lower (∼50%) than in controls. In conclusion, repeated antenatal glucocorticoid treatment programs HPA function in a sex-specific manner, and these changes are associated with modification of corticosteroid receptor expression in the adult brain and pituitary.


1981 ◽  
Vol 240 (6) ◽  
pp. E656-E661 ◽  
Author(s):  
J. C. Rose ◽  
P. J. Meis ◽  
M. Morris

We studied the ACTH, vasopressin (AVP), and cortisol responses to nitroprusside-induced hypotension in 27 chronically cannulated lamb fetuses between 0.53 and 0.98 gestation. Age-related differences in the hormonal responses to hypotension were found. Hypotension was associated with peak AVP levels of 7.8 +/- 2.7 pg/ml (mean +/- SE) in animals less than 0.68 gestation and 63.5 +/- 20 pg/ml in animals 0.89–0.98 gestation (P less than 0.05). The peak ACTH response was 95 +/- 20 pg/ml in the youngest animals and 380 +/- 111 pg/ml in animals 0.83–0.88 gestation (P less than 0.05). These observations suggest that maturation of the systems (possibly neuroendocrine) subserving the hormonal responses occurs in utero. Fetal plasma cortisol levels did not increase in response to the increase in ACTH except in animals 0.89–0.98 gestation. At this time, the basal plasma cortisol levels were high (58.8 +/- 16.8 pg/ml) and the ACTH response to hypotension was attenuated. Taken together, these findings suggest functional negative feedback regulation of ACTH by cortisol in the late gestation fetus.


1980 ◽  
Vol 87 (3) ◽  
pp. 455-461 ◽  
Author(s):  
A. EL HANI ◽  
M. DALLE ◽  
P. DELOST

Sexual dimorphism in adrenal activity appeared during the pubertal period of the guinea-pig with plasma levels and binding of cortisol lower in male guinea-pigs compared with female, and metabolic clearance rate (MCR) of cortisol higher in male than in female animals. Gonadectomy of female guinea-pigs did not change the values of the parameters regulating adrenal activity. Castration of male guinea-pigs caused a rise in plasma cortisol levels by increasing the binding capacity of transcortin for cortisol and by decreasing cortisol MCR. Treatment of females with testosterone from day 24 produced a drop on day 50 in plasma cortisol levels following a decreased binding capacity of transcortin for cortisol and at the same time as cortisol MCR increased. Furthermore, the adrenal response to stress was higher in castrated than in control males and lower in testosterone-treated females compared with control females. Testosterone appeared to be the hormone responsible for sexual dimorphism in adrenal activity in the pubertal guinea-pig.


1998 ◽  
Vol 274 (2) ◽  
pp. R445-R452 ◽  
Author(s):  
Eugenie R. Lumbers ◽  
C. Bernasconi ◽  
J. H. Burrell

To study the effects of elevated maternal levels of adrenocorticotropic hormone (ACTH) on the fetus, nine chronically catheterized pregnant ewes (132 ± 0.9 days of gestation) were infused intravenously for 3 days with Synacthen (5 μg ⋅ kg−1 ⋅ day−1). Four ewes were given 0.15 M saline intravenously over the same period. ACTH induced hypertension in the ewe. Mean arterial pressure (MAP) increased from 101 ± 4.4 to 114 ± 3.9 mmHg at 48 h ( P < 0.05); cardiac output increased from 8.6 ± 0.5 to 10.4 ± 1.0 l/min after 24 h ( P < 0.05). Within 2–4 h, maternal cortisol levels increased from 24.6 ± 6.3 to 287 ± 30 nM ( P < 0.05) and remained high. Fetal plasma cortisol levels increased from 20 ± 4.5 to 60 ± 4.5 nM ( P < 0.05) within 2–4 h and then increased further. Fetal MAP was increased at 24 h. There was no effect on fetal blood gases or pH. Ewes became hyperglycemic and lactacidemic by 24 h ( P < 0.05), and the fetuses were also hyperglycemic and lactacidemic ( P < 0.05) at this time. There were no changes in fetuses carried by saline-infused ewes. Both ewes and fetuses had raised plasma osmolalities and, since hematocrit fell, retained fluid. Ewes became hypokalemic; the fetuses did not, but there was an increase in fetal K excretion. Thus ACTH-induced hypertension in the ewe had minimal effects on fetal MAP, fetal blood gas status, and pH. The fetus, however, did show many of the other effects of maternal glucocorticoid and mineralocorticoid excess, partly because its cortisol levels were increased but also as a consequence of metabolic and endocrine changes in the ewe.


1989 ◽  
Vol 67 (11) ◽  
pp. 2746-2750 ◽  
Author(s):  
M. M. Vijayan ◽  
J. F. Leatherland

Coho salmon given intraperitoneal implants of hydrogenated coconut oil alone or coconut oil containing cortisol at 1, 5, or 10 mg/fish exhibited dose-related increases in plasma cortisol levels at day 15. After 30 days, plasma cortisol levels were significantly higher in the cortisol-implanted groups but there was no dose-related response. Plasma T3 levels were lowered in cortisol-treated fish, but plasma T4 levels were not consistently affected. Plasma glucose levels were significantly higher in the group treated with cortisol at 10 mg/fish than in the controls on both sampling days, whereas liver glycogen content and hepatosomatic index were significantly lower in the cortisol-treated groups at day 30 but not at day 15. Plasma protein levels were not significantly different between treatments at either sampling time. The splenosomatic indices were not significantly different in the three treatment groups at day 15, but at day 30 the values in the 5 and 10 mg/fish cortisol-treated groups were significantly higher than in the controls.


2002 ◽  
Vol 172 (3) ◽  
pp. 527-534 ◽  
Author(s):  
KA Clarke ◽  
JW Ward ◽  
AJ Forhead ◽  
DA Giussani ◽  
AL Fowden

The effect of fetal cortisol on the activity of the type 2 isoform of the enzyme, 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD2), was examined in ovine placenta and fetal kidney by measuring tissue 11 beta-HSD2 activity during late gestation when endogenous fetal cortisol levels rise and after exogenous cortisol administration to immature fetuses before the prepartum cortisol surge. Placental 11 beta-HSD2 activity decreased between 128-132 days and term (approximately 145 days of gestation) in association with the normal prepartum increase in fetal plasma cortisol. Raising fetal cortisol levels to prepartum values in the immature fetus at 128--132 days of gestation reduced placental 11 beta-HSD2 activity to term values. In contrast, 11 beta-HSD2 activity in the fetal renal cortex was unaffected by gestational age or cortisol infusion. When all the data were combined, there was an inverse correlation between the log fetal plasma cortisol level at delivery and placental 11 beta-HSD2 activity, expressed both on a weight-specific basis and per mg placental protein. Fetal cortisol therefore appears to be a physiological regulator of placental, but not renal, 11 beta-HSD2 activity in fetal sheep during late gestation. These findings have important implications, not only for glucocorticoid exposure in utero, but also for the local actions of cortisol within the placental tissues that are involved in initiating parturition in the sheep.


1994 ◽  
Vol 54 (1) ◽  
pp. 297-298
Author(s):  
C.C. Taylor ◽  
Y. Soong ◽  
D.L. Wu ◽  
H.H. Szeto

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