Ibrahim M M, Thomas M L, Forte L R
Biol Neonate. 1984;46(2):89-97. doi: 10.1159/000242038.
We studied the role of the parathyroids in the adaptation of intestinal Ca transport that occurs during pregnancy, and whether maternal hypoparathyroidism causes fetal hyperparathyroidism. Serum Ca of pregnant parathyroidectomized (PTX) rats was significantly greater than nonpregnant, PTX animals. Intestinal active Ca transport was increased 2.1- and 2.2-fold by pregnancy in intact and PTX rats, respectively. Serum levels of immunoreactive parathyroid hormone (PTH) were nondetectable in PTX-pregnant rats. Fetuses from PTX rats appeared grossly normal. The serum PTH was not different in fetuses from PTX compared to fetuses from intact mothers and serum Ca, Mg, and P were normal. Thus, alleviation of maternal hypocalcemia during pregnancy in PTX rats may be due to an adaptive increase in intestinal Ca transport, which does not require the parathyroids. Fetuses from PTX mothers were euparathyroid and were protected from Ca deficiency during pregnancy.
我们研究了甲状旁腺在孕期肠道钙转运适应性过程中的作用,以及母体甲状旁腺功能减退是否会导致胎儿甲状旁腺功能亢进。怀孕的甲状旁腺切除(PTX)大鼠的血清钙显著高于未怀孕的PTX动物。完整大鼠和PTX大鼠的肠道活性钙转运在孕期分别增加了2.1倍和2.2倍。PTX怀孕大鼠的血清免疫反应性甲状旁腺激素(PTH)水平检测不到。PTX大鼠的胎儿外观大体正常。与来自完整母亲的胎儿相比,PTX大鼠胎儿的血清PTH没有差异,血清钙、镁和磷均正常。因此,PTX大鼠孕期母体低钙血症的缓解可能是由于肠道钙转运的适应性增加,这并不需要甲状旁腺。PTX母亲的胎儿甲状旁腺功能正常,在孕期可免受钙缺乏的影响。