J. Lefaivre

Regulation of Growth Hormone Release in Fetal Calves

Plasma GH and IGF1 concentrations were measured during the last 2 months of gestation in 9 chronically catheterized fetal calves under basal conditions or following growth-hormone-releasing factor (GRF), thyrotropin-releasing hormone (TRH) or SRIF intravenous cotyledonnary injections. Plasma GH concentrations were higher in fetuses (1.40 +/- 0.10 nmol/l) than in dams (0.14 +/- 0.01 nmol/l). Plasma GH secretory profile was pulsatile. The number of secretory pulses, as well as their magnitude and mean baseline values decreased from 220 to 270 days of gestation. Synthetic 1-29 GRF or TRH increased fetal plasma GH concentration at 250 and 270 days of gestation but was devoid of any significant effect at 220 days. SRIF injection decreased plasma GH concentration in 270-day-old fetuses. Plasma IGF1 concentrations were lower in fetuses than in dams. No treatment had a significant effect on fetal and maternal IGF1 levels.

Foetal plasma magnesium levels during maternal hypo- or hypermagnesaemia in ewes

1. The influence of maternal hypo- or hypermagnesaemia of foetal plasma magnesium levels was studied in pregnant ewes between the 120th and the 145th day of gestation using a permanent catheter inserted in utero into the left aorta of the foetus on the 115th day of gestation. 2. In seven ewes, carrying eleven foetuses, the injection of 1 alpha-hydroxycholecalciferol induced a hypomagnesaemia which lasted 72 h. This had no significant effect on foetal plasma Mg levels. 3. In five ewes, carrying six foetuses, hypermagnesaemia induced by a 2 h magnesium chloride infusion had no significant effect on foetal plasma Mg levels. 4. These results provide evidence that in sheep during the last 20 d of gestation the foetal regulation of plasma Mg is independent of the maternal plasma Mg levels.

Endocrine Regulation of Plasma Phosphate in Sheep Fetuses with Catheters Implanted in utero

Before term, in rodents (1, 2), ruminants (3, 4, 5, 6) and humans (7), phosphatemia is higher in the fetus than in the mother. This difference of concentration between both sides of the placenta is poorly understood. In rats, it has been demonstrated that the placental transfer of 32P increased between the 19th day of gestation and term (1). In the same time fetal phosphatemia increased from 8.75 to 9.97 mg/dl (2). Calcitonin injection in fetal rats (8) and in fetal monkeys (9) induced a significant hypocalcemia and hypophosphatemia in the fetus. In rat fetuses treated with parathyroid extract intravenously or subcutaneously calcemia was increased while phosphatemia was lower than in fetuses injected with the vehicle alone (10). In acute preparations of sheep fetuses, the intravenous infusion of parathyroid extract (0.1 I.U./kg/mn during 1 hr) increased promptly and significantly the renal phosphate-glomerular filtration rate clearance ratio, while the glomerular filtration rate, serum calcium, serum phosphate and filtered load of phosphate did not change significantly (4). In fact the endocrine regulation of fetal phosphatemia remains obscure.The purpose of this investigation was to study the effects of calcitonin, parathyroid hormone, 1α-hydroxycholecalciferol and 5,6 trans-25 hydroxycholecalciferol, injected intravenously in unstressed fetal lambs, on fetal and maternal phosphatemia, calcemia and magnesemia.