Effect of β-adrenergic blockade on lung liquid secretion during fetal asphyxia

The hypothesis tested in this study was that β-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the β-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 ± 1.0 to 1.5 ± 0.4 ml/h (P < 0.001) by RUBF; the administration of propranolol had no further effect on these liquid production rates (1.1 ± 0.5 ml/h). In other experiments epinephrine infusion reduced the net production rate of fetal lung liquid from a mean control value of 7.2 ± 1.4 to 1.7 ± 1.8 ml/h (P < 0.025); the addition of propranolol reversed this inhibition (secretion rate 6.1 ± 1.4 ml/h, P < 0.005). We conclude that the inhibition of fetal lung liquid production induced by moderate fetal asphyxia does not solely result from catecholamine stimulation of pulmonary β-receptors.