Pitkin R M, Reynolds W A, Williams G A, Kawahara W, Bauman A F, Hargis G K
J Clin Endocrinol Metab. 1980 Nov;51(5):1044-7. doi: 10.1210/jcem-51-5-1044.
Maternal and fetal parathyroidd hormone (PTH) responsiveness to hypocalcemia induced by EDTA infusion (50 mg/kg over 2 h) was studied in rhesus monkeys in late pregnancy. Although baseline serum total calcium (Ca) levels in the fetus exceeded those in the mother (4.83 +/- 0.13 vs. 4.28 +/- 0.15 meq/liter; P < 0.001), PTH values were not significantly different (5.62 +/- 0.37 vs. 6.18 +/- 0.33 muleq/ml; P > 0.05). EDTA infusion directly to five fetuses produced significant hypocalcemia (maximal decline averaging 19 +/- 2%) and PTH response (maximal increase averaging 46 +/- 5%). In contrast, in four control studies involving fetal saline infusion, there were no significant changes in fetal Ca or PTH levels. Four maternal control infusions produced no significant changes in either Ca or PTH levels. A comparison of maternal and fetal PTH responses indicated considerable similarity, although fetal PTH levels tended to return to baseline somewhat more gradually after cessation of the hypocalcemic stimulus than did maternal levels. These studies indicate that fetal PTH secretion, both baseline and in response to hypocalcemia, is quantitatively similar to that of the adult, and thus, the fetal parathyroid does not appear to be suppressed by the relative hypercalcemia of late fetal life.
在妊娠晚期的恒河猴中,研究了母体和胎儿甲状旁腺激素(PTH)对乙二胺四乙酸(EDTA)输注(2小时内输注50mg/kg)诱导的低钙血症的反应。尽管胎儿的基线血清总钙(Ca)水平超过母体(4.83±0.13对4.28±0.15mEq/升;P<0.001),但PTH值无显著差异(5.62±0.37对6.18±0.33mUeq/ml;P>0.05)。直接向五只胎儿输注EDTA导致显著的低钙血症(最大下降平均为19±2%)和PTH反应(最大增加平均为46±5%)。相比之下,在四项涉及胎儿输注生理盐水的对照研究中,胎儿的Ca或PTH水平没有显著变化。四项母体对照输注对Ca或PTH水平均无显著影响。母体和胎儿PTH反应的比较表明有相当大的相似性,尽管在低钙血症刺激停止后,胎儿PTH水平恢复到基线的速度比母体水平略慢。这些研究表明,胎儿PTH的分泌,无论是基线水平还是对低钙血症的反应,在数量上与成人相似,因此,胎儿甲状旁腺似乎没有受到胎儿晚期相对高钙血症的抑制。