Distention-produced phospholipid secretion in postmortem in situ lungs of newborn rabbits. Inhibition by specific beta-adrenergic blockade.

The secretion of total phospholipid in postmortem in situ lungs of newborn rabbits was examined using the technique of lung lavage after an initial lavage procedure, and then after a period of static air inflation at 30 cm H2O pressure for 45 min. There was a significant reduction in the phospholipid yield with 10(-3) molar DL-propranolol used as the initial lavage fluid, both immediately after the initial lavage procedure (experimental group, 0.29 +/- SE 0.04 mg/g dry lung weight; control group, 0.57 +/- SE 0.09; p less than 0.01) and after static inflation with air (experimental group, 1.14 +/- SE 0.15; control group, 2.22 +/- SE 0.24; p less than 0.001). Preinjection of the breathing newborn rabbit with DL-propranolol was not necessary for this inhibitory effect. There was no significant reduction when 10(-3) molar atropine, lidocaine, D-propranolol, or 10(-5) scopolamine were substituted as the initial lavage fluid, nor was there any reduction when the concentration of DL-propranolol was decreased to 10(-4) or 10(-5) molar. Because D-propranolol has all the properties of DL-propranolol, except 100-fold less beta-adrenergic antagonist activity, the inhibition by propranolol was due to specific beta-adrenergic blockade. In the absence of an intact circulation or a functional central nervous system, it is concluded that surfactant phospholipid secretion is partly controlled by an intrapulmonary neurogenic reflex.