Development of beta-adrenergic control of phospholipid secretion in rabbit lung

Lung distension is associated with increased phospholipid secretion into the air spaces. Basal, lavage-induced, and inflation-produced phospholipid secretion, in postmortem in situ lungs of newborn rabbits, were examined at three different levels of maturity, with and without 10(-3) M dl-propranolol. Lungs were lavaged with saline at successive 3- and 15-min time intervals to separate basal from lavage-induced secretion. Inflation-produced secretion was studied after static inflation at 30 cmH2O for 30 min. At 27.5 days gestation, basal secretion was undetectable, and neither lavage-induced nor inflation-produced secretion were influenced by propranolol. At 29.5 days gestation, basal secretion was only just detectable. Distension-associated secretion was increased over that present at 27.5 days gestation, and propranolol had a significant inhibitory effect, especially on lavage-induced secretion, in which the inhibition was shown to be rapidly reversible. There was a significant increase of basal secretion at 2.5 days postterm, possibly inhibited by propranolol. In addition, there was a further substantial increase of distension-associated secretion, and the inhibitory effect of propranolol persisted. These changes were independent of the sedimentation behavior of lavaged phospholipid. Overall, the results are consistent with evidence, produced in other laboratories, that there is an increasing density of sympathetic neurons and beta-adrenergic receptors in whole lung preparations during late gestation in the rabbit and suggest that granular pneumocytes, the presumed source of secreted phospholipid, take part in this developmental change.