We correlated the ontogeny of pulmonary beta-adrenergic receptors with the onset of surface active material (SAM) flux into tracheal fluid of male and female chronically catheterized fetal lambs. SAM flux began between 0.82 and 0.85 gestation in the females and between 0.85 and 0.89 gestation in the males and matured more rapidly thereafter in the females than in the males (P less than 0.01). beta-Adrenergic receptor binding, using [3H]dihydroalprenolol as the ligand, was saturable, linear, and stereospecific. The order of potency of competitive beta-agonists was isoproterenol greater than norepinephrine greater than epinephrine. The maximal binding capacity (Bmax) of pulmonary beta-receptors approximately doubled between 0.84 and 0.89 gestation, coinciding with the onset of SAM flux. Bmax matured as a third degree polynomial function of gestational age in females (r = 0.9, P less than 0.001) but as a linear function in males (r = 0.8, P less than 0.005). Between 0.86 and 0.93 gestation, Bmax was 1.45-fold greater in females than males (P less than 0.001). The dissociation constant of beta-receptors was not influenced significantly by gender or gestation. We conclude that maturation of pulmonary beta-receptors coincides with the onset of SAM flux in fetal lambs and that both mature more rapidly in females. We speculate that pulmonary beta-receptor maturation and SAM flux are coregulated by hormonal factors. More rapid maturation of pulmonary beta-receptors and SAM flux in females may be a factor in the female advantage with regard to pulmonary surfactant maturation and the survival of premature neonates.
Chronic Hyperglycemia Reduces Surface Active Material Flux in Tracheal Fluid of Fetal Lambs