Abstract

To study the effects of beta-2 agonist on tracheal fluid, surfactant and pulmonary mechanics in fetal lamb lung, ritodrine hydrochloride, a preferential beta-2 agonist, was infused i.v. at a rate of 1.3 +/- 0.4 micrograms/kg/min (mean +/- S.D.) for 24 hr into six twin chronically catheterized fetal lambs starting between 0.86 and 0.91 gestation. Ritodrine infusion was associated with statistically significant metabolic and pulmonary effects in comparison with twin controls. Fetal serum glucose levels were elevated 1.7-fold, arterial blood pH fell 0.04 U and arterial blood pO2 fell 5.1 torr in the ritodrine-infused twins. Tracheal fluid flow was reduced 6.9-fold and surface active material flux into the tracheal fluid was thereby virtually eliminated. But the surface active material content of tracheal fluid and lung lavage increased 3.0-fold. The surfactant phospholipid content of lung lavage also increased 3.0-fold with no change in its composition. There was a concomitant improvement in pulmonary mechanics on pressure-volume curves: the lungs of the ritodrine-infused twins filled with 1.7-fold more air on inflation to 40 cm of water pressure and also retained 1.7-fold more air on deflation to 10 cm of water pressure. We conclude that beta-2 agonist inhibits tracheal fluid flow, increases surfactant in lung lavage and improves lung stability in the fetal lamb lung. We speculate that preferential beta-2 adrenergic stimulation of the fetal lung with ritodrine could be helpful in the prevention of neonatal respiratory distress syndrome because of enhanced surfactant availability in airways and improved pulmonary mechanics.