Prenatal glucocorticoid (GC) treatment increases fetal thyroid hormone (TH) activity in humans and in animals. Though it is postulated that this increase in fetal TH activity after GC therapy plays an important role in accelerating fetal lung maturation, this hypothesis remains unproven. In the hyt/hyt mouse primary hypothyroidism occurs dut to a mutation in the β subunit of the TSH receptor of the thyroid gland. Primary hypothyroidism is transmitted as an autosomal recessive trait. We studied the effect of maternal GC therapy on lung ultrastructural maturation in the hyt/hyt mouse fetus. hyt/hyt mice made euthyroid by T3 supplementation were mated to carry hyt/hyt pups. Balb-c mice served as controls. Vehicle or Betamethasone (Beta., Celestone, 0.1 ml/dose) was injected (I.P., b.i.d.) into the pregnant mice on d 16 and 17 of gestation(vaginal plug=1 d, term ≈20 d). All mice were killed on d 18 of pregnancy. Fetal lungs were subjected to morphometric analysis using the Chalkey point counting system with an an interactive computerized image analyzer (Optimas, Bioscan). All data X ± SEM * P < 0.05 vs control. LB=Lamellar Bodies. Table
Fetal lungs of Balb-c mice treated with Beta but not the vehicle showed plenty of tubular myelin (TM). Though the number of LB and alveolar/parenchymal ratio in the fetal lungs of Beta treated hyt/hyt mice increased significantly, TM was conspicuously absent in these lungs. CONCLUSION Fetal thyroid plays an important role in acceleration of fetal lung maturation from GC stimulation. (NIH-HL-52839).
