Theodoropoulos T J
Endocrinology. 1985 Oct;117(4):1683-6. doi: 10.1210/endo-117-4-1683.
The perinatal rat exhibits low serum TSH levels in the presence of very low concentrations of T3 and T4. We had reported previously that this animal does not require endogenous TRH for TSH release. We investigated here whether the inhibitory hormone somatostatin (SS) has a role in maintaining the low TSH secretory set-point. To study the effect of SS in the immature model, we passively immunized pregnant rats with SS antiserum to neutralize endogenous SS. Acute iv administration of 0.3 ml SS antiserum to pregnant rats (day 20 of pregnancy) resulted in a significant serum TSH elevation in both mother and fetus 60 min after injection compared to the control values [maternal TSH, 62 +/- 6 muU/ml vs. control, 43 +/- 4 (mean +/- SE; P less than 0.05); fetal TSH, 95 +/- 8 vs. control, 66 +/- 6 (P less than 0.02)]. The binding capacity of the AS in the fetal serum far exceeded the circulating SS in the fetus. Similar results were obtained when neonates 5 and 10 days of age were injected with 0.1 ml AS, ip. Further experiments were done with the use of synthetic SS. Acute iv injection of synthetic synthetic SS (1 microgram) to pregnant rats made hypothyroid by feeding of a low iodine-propylthiouracil diet for the last week of gestation suppressed the elevated serum TSH level in both mother and fetus 15 min after the injection [maternal TSH, 102 +/- 11 vs. control, 163 +/- 22 (P less than 0.05); fetal TSH, 99 +/- 9 vs. control, 143 +/- 13 (P less than 0.02)]. Similar results were obtained when hypothyroid neonates 5 and 10 days of age were injected with 1 microgram SS, ip. These findings suggest that there is similarity in the effects of SS on TSH secretion (suppression) in mother, fetus, and neonate and dependence of the perinatal TSH on SS, in contrast to TRH. It is, then, likely that TSH secretion in the perinatal rat is under the inhibitory influence of endogenous SS.
围产期大鼠在极低浓度的T3和T4存在时血清促甲状腺激素（TSH）水平较低。我们之前曾报道，这种动物促甲状腺激素释放不需要内源性促甲状腺激素释放激素（TRH）。我们在此研究抑制性激素生长抑素（SS）是否在维持低促甲状腺激素分泌设定点方面发挥作用。为了研究SS在未成熟模型中的作用，我们用SS抗血清被动免疫怀孕大鼠以中和内源性SS。在怀孕大鼠（妊娠第20天）静脉内急性注射0.3 ml SS抗血清，与对照值相比，注射后60分钟母体和胎儿的血清TSH均显著升高[母体TSH，62±6 μU/ml对对照，43±4（平均值±标准误；P<0.05）；胎儿TSH，95±8对对照，66±6（P<0.02）]。胎儿血清中抗血清（AS）的结合能力远远超过胎儿循环中的SS。当给5日龄和10日龄的新生儿腹腔注射0.1 ml AS时，也获得了类似的结果。使用合成SS进行了进一步实验。在妊娠最后一周通过喂食低碘-丙硫氧嘧啶饮食使怀孕大鼠甲状腺功能减退，静脉内急性注射合成SS（1微克），注射后15分钟母体和胎儿血清TSH升高水平均受到抑制[母体TSH，102±11对对照，163±22（P<0.05）；胎儿TSH，99±9对对照，143±13（P<0.02）]。当给5日龄和10日龄甲状腺功能减退的新生儿腹腔注射1微克SS时，也获得了类似的结果。这些发现表明，SS对母体、胎儿和新生儿促甲状腺激素分泌（抑制）的作用存在相似性，且围产期促甲状腺激素对SS存在依赖性，这与TRH不同。因此，围产期大鼠的促甲状腺激素分泌可能受内源性SS的抑制影响。
