Effect of Fetal Decapitation on Unbound Rat Plasma Corticosterone Concentration at the End of Pregnancy

Neonatology ◽  
1985 ◽  
Vol 47 (3) ◽  
pp. 163-169 ◽  
Author(s):  
Alia Cohen ◽  
Yveline Guillon
1975 ◽  
Vol 53 (3) ◽  
pp. 475-478 ◽  
Author(s):  
William Rotsztejn ◽  
Josée Lalonde ◽  
Maurice Normand ◽  
Claude Fortier

Advantage was taken of a specific and sensitive bioassay for rat plasma adrenocorticotropin (ACTH) based on the dispersion of rat adrenal cells with trypsin, to investigate the relationship between plasma corticosterone concentration and inhibition of ACTH release under steady-stale conditions achieved by graded rates (0–5.12 μg/min per 100 g body weight) of intravenous infusion of the steroid for 45 min in 28-day adrenalectomized rats. In contrast to prior reports involving suppression of stress-induced ACTH release, the inhibitory effect of corticosterone was shown, under our experimental conditions, to be exerted also on the basal rate of ACTH secretion. Indeed, a slight though not significant decrease of plasma ACTH concentration was observed with the corticosterone infusion rate of 0.64 μg/min per 100 g body weight, and further progressive and highly significant drops in concentration were recorded for infusion rates of 2.56 and 5.12 μg/min per 100 g body weight. An increase of the metabolic clearance rate of corticosterone, observed as a function of the infusion rate, was ascribed to saturation by the steroid of the plasma transcortin binding sites.


1977 ◽  
Vol 73 (2) ◽  
pp. 347-353 ◽  
Author(s):  
R. N. BARTON

SUMMARY In post-absorptive rats in a 20 °C environment, bilateral hind-limb ischaemia decreased the plasma growth hormone concentration below the very wide range found in control rats. Injection of sodium pentobarbitone increased the concentration in both control and injured rats but did not eliminate the difference between them. A 20% dorsal scald also decreased the variability of plasma growth hormone concentration but did not reduce it below the normal range. Thus growth hormone is probably not responsible for the insulin resistance seen in the severely injured rat. The plasma corticosterone concentration markedly increased after both injuries but was not altered by pentobarbitone.


1986 ◽  
Vol 112 (3) ◽  
pp. 396-403 ◽  
Author(s):  
Jean Paul Dupouy ◽  
Alain Chatelain

Abstract. CBG and pituitary-adrenal activities were investigated in intact rat foetuses, in newborns spontaneously delivered by vaginal way and in postmature foetuses from mothers with delayed parturition caused by daily progesterone injection from day 20 of gestation. The postmature foetuses had lower body weights and higher adrenal weights on day 22, 23 and 24 of gestation than newborns of the same conceptional age. The corticosterone binding capacity of the plasma as well as the binding capacity of CBG for corticosterone decreased in intact foetuses for the last 3 days of gestation and stayed very low in pups from day 0 to day 8 postpartum. These parameters decreased more slowly in postmature foetuses; however, the differences between the latter and intact foetuses or newborns were not statistically significant. Similar evolution occurred in intact pregnant and suckling females as well as in females with prolonged gestation. The fall in CBG activity in normal rat pups and the subsequent rise in free steroids could explain a sharp decrease in plasma ACTH levels as well as the drop in adrenal and plasma corticosterone concentration. In foetuses with prolonged gestation, the same phenomenon did not occur. Stress conditions produced by maintaining growing foetuses in utero and the development of severe jaundice maintained high ACTH levels. In contrast, the fall in adrenal and plasma corticosterone concentrations in spite of the high level of circulating ACTH could be mainly due to the progesterone inhibition of the steroidogenic activity of the foetal adrenals.


1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine

These experiments were undertaken to investigate the mechanism whereby a precipitous drop in plasma corticosterone concentration is brought about following drinking in rats on a restricted water schedule. No alteration in adrenocorticotrophic hormone (ACTH) output was found, nor was catabolism of corticosterone sufficient to account for the drop. It is concluded that corticosterone level is controlled under these conditions by a mechanism independent of ACTH concentration.


1974 ◽  
Vol 63 (1) ◽  
pp. 213-222 ◽  
Author(s):  
JULIA C. BUCKINGHAM ◽  
J. R. HODGES

SUMMARY Changes in pituitary and plasma corticotrophin (ACTH), estimated by redox bioassay, were correlated with changes in plasma corticosterone in adrenalectomized rats, with and without corticosterone treatment, before and after exposure to stress. After adrenalectomy, the plasma ACTH concentration was persistently increased. The pituitary ACTH content declined and then increased markedly. These changes were prevented by physiological doses of corticosteroids. Stress caused only a small rise in the plasma ACTH concentration in intact and sham-operated rats but a marked increase in adrenalectomized animals. This exaggerated response was reduced to normal by physiological doses of corticosterone. Prolonged treatment with higher doses of corticosterone was necessary to abolish completely the adrenocorticotrophic response to stress. However, one injection of the steroid, in a dose sufficient to raise the plasma corticosterone concentration to a similar level, did not impair the stress-induced release of ACTH. The results suggest that the synthesis and the basal release of ACTH are directly controlled by the concentration of corticosteroid in the blood, but the corticosteroids exert only a delayed effect in modulating the stress-induced release of the hormone.


1977 ◽  
Vol 43 (5) ◽  
pp. 839-843 ◽  
Author(s):  
J. A. Severson ◽  
R. D. Fell ◽  
J. G. Tuig ◽  
D. R. Griffith

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone were determined in exercise-trained rats. Rats, 100, 200, and 300 days of age, were trained for a 10-wk period by treadmill running. Following the training program, rats were subjected to an acute bout of swimming. Acute swimming elevated plasma corticosterone concentrations in all age groups. At 170 days of age, the plasma corticosterone concentration following swimming was higher in exercise-trained rats than in controls. The opposite was true of acutely swum rats at 270 and 370 days of age. Acute swimming elevated the in vitro adrenal gland response to adrenocorticotropic hormone stimulation in control rats at all ages and in trained rats at 170 days of age. The in vivo relationship of epinephrine and the pituitary adrenal system is suggested as a mechanism which could have caused this response. The relationship of secretion rates to plasma corticosterone concentrations indicated that extra-adrenal mechanisms, such as decreased turnover, were also responsible for the elevated plasma corticosterone levels observed in response to acute swimming.


1988 ◽  
Vol 119 (3) ◽  
pp. 339-344 ◽  
Author(s):  
Jon D. Dunn ◽  
Jerald J. Killion

Abstract. We previously have shown that melittin evokes a sustained increase in plasma corticosterone levels of the female rat. Significant increases occurred only during the morning and the duration of the response was increased from 48 h to 8 days by a second milittin injection 3 days after initial exposure to melittin. To further evaluate the effect of melittin on adrenocortical function, rats were given melittin at 09.00 h on days 1 and 4 and on day 8 rats were subjected to a variety of different stresses. Saline-injected rats served as controls. Blood for determining non-stress and stress levels of corticosterone concentration (RIA) was collected by decapitation. In all cases morning but not afternoon non-stress plasma corticosterone levels of melittin-injected rats were higher than those of saline-injected controls; afternoon non-stress corticosterone levels did not differ between groups. Melittin- and saline-treated rats showed comparable corticosterone responses to a morning 2-min restraint stress. In contrast, melittin treatment facilitated the pituitary-adrenal response to rotational and surgical stress as well as the stress of removing one rat from a cage of two. Fifteen min after removal of the first rat of a cage of two, plasma corticosterone levels of the melittin-injected rat were significantly higher than those of saline-injected rats. Likewise, plasma corticosterone levels of melittin-treated rats were higher (P < 0.05) than those of saline-injected rats 15 min after rotational (10 rpm) and surgical (jugular cutdown and blood withdrawal) stress. Collectively these data indicate that exposure to melittin (and/or the resulting increase in morning corticosterone levels) may have a significant influence on the pituitary-adrenal responsiveness to stress.


1972 ◽  
Vol 52 (3) ◽  
pp. 435-450 ◽  
Author(s):  
MO YIN CHAN ◽  
E. L. BRADLEY ◽  
W. N. HOLMES

SUMMARY The distribution and disappearance of radioactivity after the intravenous administration of [1,2-3H]corticosterone and [1,2-3H]aldosterone to the pigeon were studied according to one- and two-compartment model systems. The volume of distribution (AVD) of the total and methylene chlorideextractable radioactivity in the plasma of hypophysectomized pigeons injected with labelled corticosterone was significantly increased. Also the biological half-life (T½) of each radioactive fraction in plasma was significantly prolonged. No significant change in the metabolic clearance rate (MCR) of labelled corticosterone was observed in the hypophysectomized pigeon. The AVD of the total and methylene chloride-extractable tritium in the plasma of the hypophysectomized pigeon injected with labelled aldosterone was unchanged but the T½ of both plasma fractions was significantly prolonged. The estimated MCR of labelled aldosterone was significantly diminished. The concentration of total fluorogenic corticosteroid in plasma from the chronically hypophysectomized pigeon was reduced to one-third of that in the sham-operated bird, and corticotrophin-replacement therapy restored the concentration to normal. After hypophysectomy, the plasma corticosterone concentration was reduced to 20% of the concentration in the sham-operated birds, and replacement therapy with corticotrophin again restored the plasma levels to normal. Estimation of the endogenous corticosterone secretory rates indicated that chronic hypophysectomy was accompanied by a decline commensurate with the reduction in the plasma corticosterone concentration.


1990 ◽  
Vol 258 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. R. Gwosdow ◽  
M. S. Kumar ◽  
H. H. Bode

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)


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