Abstract
Propyl-thiouracil (PTU) feeding of pregnant guinea pigs during the last several weeks of gestation resulted in progressive fetal thyroid hyperplasia (13- to 50-fold). TSH [thyroid-stimulating hormone] concentrations of plasma and pituitary were significantly elevated in goitrous offspring. The elevation in TSH levels was closely correlated with the appearance in the fetal pars distalis of numerous, glycoprotein granulated, enlarged basophils. Maternal titers of plasma TSH were also increased, but structural changes in thyroid and hypophysis were minimal unless goitrogen treatment was prolonged. The delay in goitrogenesis of adult animals was also observed in normal newborn. PTU administration during the first 2 weeks of life failed to induce significant histological change in the thyroid or to alter TSH levels in blood and pituitary. Daily sc injections of thyroxine (T4) or triiodothyronine (T3), at high dose levels, for 3-9 days, into pregnant animals substantially reduced TSH stores in the adenohypophysis but had no demonstrable effect on the pituitary-thyroid system of their offspring. T4 administration to normal neonates throughout the first postnatal week was effective in suppressing THS secretion, as judged by reduction in thyroid and pituitary weight and lowered TSH concentrations. It is concluded that in the guinea pig deficiency of thyroid hormone or TSH excess in the mother has little or no appreciable effect on the pituitary-thyroid axis of the fetus. The fetal hypophysis has the capacity to augment TSH secretion in response to chemical thyroidectomy induced by antithyroid agents. The results also strongly suggest that the hypophysial-thyroid system functions at a higher level in late fetal than in early postnatal life.