| pubmed-article:1352752 | pubmed:abstractText | To study the effects of hyperoxia and beta-adrenergic stimulation on pulmonary surfactant in the neonatal lung, we measured disaturated phosphatidylcholine (DSPC) and [14C]choline incorporation into DSPC, obtained from alveolar lavage and lung tissue. We used an isolated salt-perfused rabbit lung preparation from neonatal rabbits exposed to room air or greater than 95% oxygen for 3 days. There were four experimental groups: room air, basal condition; room air, beta-adrenergic stimulation; hyperoxia, basal conditions; and hyperoxia, beta-adrenergic stimulation. Hyperoxia caused a significant decrease in lavage and intracellular [14C]DSPC specific activity, and a decrease in intracellular DSPC suggesting depressed surfactant synthesis. Beta-stimulation in room air caused a decrease in lavage DSPC, an increase in DSPC, and [14C]DSPC fraction released, consistent with increased uptake for reutilization. With hyperoxia and beta-stimulation, there is an increase in total DSPC in the lavage; lavage [14C]DSPC specific activity is similar to that of the basal hyperoxia group (i.e., depressed compared with the room air state); intracellular [14C]DSPC specific activity does not differ from basal, hyperoxia, or beta-stimulated, room air groups, all being depressed compared with basal, room air conditions. Intracellular DSPC in the beta-stimulated group is less affected by hyperoxia than the basal groups. It appears that prolonged exposure to hyperoxia is manifested primarily by a decrease in [14C]DSPC specific activity suggesting alterations in surfactant synthesis, though DSPC in the lavage is not altered. Beta-adrenergic stimulation may enhance release of newly synthesized surfactant into the alveoli, and possibly enhances uptake for reutilization. The enhancement of surfactant release seems to be preserved after prolonged hyperoxia. | lld:pubmed |
