Plasma Calcium Control in the Rat Fetus. III. Influence of Alterations in Maternal Plasma Calcium on Fetal Plasma Calcium Level

Neonatology ◽  
1985 ◽  
Vol 48 (6) ◽  
pp. 329-335 ◽  
Author(s):  
Sylvie Chalon ◽  
Jean-Michel Garel
2008 ◽  
Vol 53 (1-4) ◽  
pp. 5-18
Author(s):  
Bhawna Srivastava ◽  
Diwakar Mishra ◽  
Sunil Srivastav ◽  
Nobuo Suzuki ◽  
Ajai Srivastav

1,25(OH)2D3Induced Alterations in Plasma Calcium, Inorganic Phosphate, Ultimobranhial Gland and Parathyroid Gland of the Garden Lizard,Calotes VersicolorGarden lizardsCalotes versicolorwere procured and given daily intraperitoneal injections of 30 pmol of 1,25(OH)2D3/50 g body wt for 30 days. Lizards were sacrificed on the 1st, 3rd, 5th, 10th, 15thand 30thday of the experiment. The plasma calcium levels ofC. versicolorremain unaffected after day 1 following 1,25(OH)2D3treatment. After day 3 the levels increase significantly which progresses up to day 10. Thereafter, the plasma calcium level tends to decrease on day 15 and the levels become normal at day 30. In 1,25(OH)2D3injected lizards the plasma inorganic phosphate levels remain unaltered up to day 3. After day 5, the value increases significantly. This increase progresses up to day 15. On day 30, the levels become almost normal. The ultimobranchial gland exhibits hyperactivity following 5 day 1,25(OH)2D3treatment which is expressed by an increase in the nuclear volume and weak staining response of the cytoplasm of ultimobranchial cells. After day 10, the nuclear volume is further increased and some of the cells are exhausted. Following 15 days 1,25(OH)2D3treatment the nuclear volume records an increase and many degenerating cells are discerned. After day 30, the nuclear volume is almost normal, most cells seem to be recovered and only a few degenerating cells are noticed. After day 10 and day 15 following 1,25(OH)2D3treatment, the parathyroid glands ofC. versicolorshow reduced chromaticity of nuclei and a progressive decrease in the nuclear volume of parathyroidal cells. On day 30, the nuclear volume tends to become normal and a few degenerating cells are observed.


1971 ◽  
Vol 68 (2_Suppla) ◽  
pp. S5-S64 ◽  
Author(s):  
Georg M. Salzer

ABSTRACT A survey of the literature of the last fifty years relating to our topic indicates that the sentence from Copp (1969) »there is no evidence that the anterior pituitary or the central nervous system has any direct effect on the secretion of parathormone or calcitonin« is not based upon concrete experimental data. This is particularly evident from a morphological aspect, since considerable variations in the parathyroids have been repeately observed as the result of both hypophysectomy and the application of hypophyseal extracts. Experimental evidence has contributed little material relevant to a possible hypophyseal control of the parathyroids with the exception of the observation that after hypophysectomy the plasma calcium level remains unchanged. Contrary to this, up to now no positive morphological changes in the C-cells of the thyroid have been determined, although experimental evidence suggests a certain hypophyseal control upon the secretion of calcitonin. All the results of our own experiments in parathyroid morphology suggest significant alterations in the glands subsequent to hypophysectomy. A histological survey shows a considerable reduction in the size of the entire organ and an increase in the connective tissue of the gland. Karyometric tests reveal a reduction of the small diameter of the nuclei of 13.5%, a quantity which corresponds to that found in the nuclei of the adrenal cortex and the follicular cells of the thyroid after the same operation. As a result of hypophysectomy it is possible under the electron microscope to distinguish alterations in the secretory structures of the parenchyma cells of the parathyroid that may indicate restricted parathormone synthesis. In order to exclude the possibility that these changes may have been conditioned by a cessation of adrenal activity, the parathyroid morphology was analyzed also after adrenalectomy. The results obtained in this way differ fundamentally from those produced by hypophysectomy. Morphometrical investigation of the C-cell population of the thyroid after hypophysectomy show a significant reduction in the size of the nuclei of 13.6 % and, under the electron microscope, a reduction of the cytoplasm as well as an increase in the number of calcitonin granula. Two further test series have shown that in hypophysectomized but otherwise untreated animals the plasma calcium level is within the normal range. On the other hand the normal ability to counteract hyper- or hypocalcaemia was found to be lacking to a great extent. All the results obtained suggest the existence of some hypophyseal influence upon the hormonal calcium regulation system. A hypothesis is framed to the effect that the feedback: plasma calcium – parathormone and calcitonin serves, above all, the purpose of compensating an alimentary over- and under-supply of calcium, whereas the hypophyseal regulatory cycle serves to meet the endogenic calcium requirements of the organism under special circumstances, as for instance growth or lactation.


1983 ◽  
Vol 99 (3) ◽  
pp. 347-353 ◽  
Author(s):  
C. Rebut-Bonneton ◽  
J. Demignon ◽  
B. Amor ◽  
L. Miravet

Fetal bone resorption was measured by an organ culture technique using fetuses from intact or thyroparathyroidectomized pregnant rats. These experiments were performed to investigate the effects of 1,25-dihydroxycholecalciferol (1,25-DHCC) and salmon calcitonin (SCT) in pregnant rats, on both fetal growth and fetal bone resorption. Pregnant rats were given 0·1–0·5 μg 1,25-DHCC per day from day 17 of gestation: in intact rats bone resorption was increased and fetal growth decreased; 1,25-DHCC probably modified fetal bone resorption in the absence of fetal parathyroid secretion. Infusion of SCT in minipumps (30 mu./h) did not modify plasma calcium levels in either the mother or fetuses, neither was bone resorption altered. In 1,25-DHCC-treated rats, SCT infusion resulted in an increase in fetal weight and a decrease in fetal bone resorption. On the other hand, SCT infusion was found to facilitate phosphate accumulation in fetuses. At the end of the SCT infusion the SCT concentration was 450 ng/l in maternal plasma and 553± 60 ng/l in fetal plasma. Salmon calcitonin was shown to cross the placental barrier in the rats; it may interact with the effects of 1,25-DHCC in the fetus.


1989 ◽  
Vol 120 (1) ◽  
pp. 20-30 ◽  
Author(s):  
Gabriella Morreale de Escobar ◽  
María Jesís Obregón ◽  
Carmen Ruiz de Oña ◽  
Francisco Escobar del Rey

Abstract. Thyroxine (T4) is transferred from the mother to the hypothyroid rat fetus late in gestation, mitigating T4 and T3 deficiency in fetal tissues, the brain included. We have now compared the effects of maternal infusion with T3. Normal and thyroidectomized rats were started on methimazole (MMI) on the 14th day of gestation, given alone, or together with a constant infusion of 0.45 μg (0.69 nmol) T3 or of 1.8 μg (2.3 nmol) T4/100 g per day. Maternal and fetal samples were obtained at the 21st day of gestation. The doses of T3 and T4 were biologically equivalent for the dams, as assessed from maternal plasma and tissue T3, and plasma TSH levels. MMI blocked the fetal thyroid; T4 and T3 levels were low in all fetal tissues, and fetal plasma TSH was high. Maternal infusion with T4 mitigated both T4 and T3 deficiency in all fetal tissues, the brain included, and decreased fetal plasma TSH. In contrast, infusion of T3 normalized fetal plasma T3 and increased the T3 levels in several tissues, but not in the brain. Neither did it decrease the high fetal plasma TSH levels. The results show that when the fetus is hypothyroid, T3 crosses the rat placenta at the end of gestation, but does not affect all tissues to the same degree. In contrast to the effects of maternal T4, maternal T3 does not alleviate the T3 deficiency of the brain or, presumably, of the thyrotrope. Thus, end-points of thyroid hormone action related to TSH release should not be used to measure transfer of maternal T3 to the fetal compartment. Moreover, T4 should be given, and not T3, to protect the hypothyroid fetal brain.


1986 ◽  
Vol 108 (3) ◽  
pp. 361-367 ◽  
Author(s):  
R. Habert ◽  
R. Picon

ABSTRACT The present study was performed to examine whether circulating progesterone regulates testicular testosterone production in the fetal rat. Progesterone levels in fetal plasma were found to increase from day 14·5 to day 16·5; thereafter they reached a plateau between days 16·5 and 18·5 (80 nmol/l) and decreased threefold between days 18·5 and 21·5. The addition of progesterone, within the range of normal plasma concentrations, induced a dose-dependent increase in testosterone produced in vitro by the testes on days 16·5 and 18·5 but not on day 20·5. However, in 18·5-day-old fetuses, individual plasma progesterone levels were not correlated with testicular testosterone production in vivo and in vitro. Furthermore, maternal bilateral ovariectomy induced a significant fall in plasma progesterone in 18·5-day-old fetuses; this was not associated with a reduction in plasma testosterone nor in testicular testosterone content, although the amount of testosterone secreted by the testis incubated in vitro was slightly but significantly reduced. It is concluded that circulating progesterone does not regulate testicular testosterone production in vivo although the testis may use plasma progesterone as a substrate. On day 18·5 after maternal ovariectomy, the decrease in plasma progesterone levels was similar in fetuses and mothers, suggesting that most fetal progesterone originates from maternal plasma. J. Endocr. (1986) 108, 361–367


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