β-adrenergic priming of rats in vivo modulates the effect of β-agonist in vitro on surfactant phospholipid metabolism of isolated lungs

Abstract

To evaluate the effects of multiple beta-adrenergic stimulations on pulmonary surfactant phospholipids, perfused lungs from beta-adrenergic primed and non-primed rats were challenged with the beta-agonist terbutaline in vitro. Cell-free lung lavage, lavagable alveolar cells and lung tissue were analysed for phospholipid content and incorporation of precursors. In lung lavage, terbutaline in vitro doubled the incorporation of 14C-choline and 3H-palmitate into total phosphatidylcholine (PC) and of 3H-palmitate into phosphatidylglycerol (PG). beta-adrenergic priming in vivo prior to terbutaline in vitro lowered the increase of precursor incorporation. For lavagable cells, terbutaline in vitro increased the incorporation of 3H-palmitate into PC. Priming in vivo reduced this effect and diminished the specific 3H-choline incorporation into lavagable cell PC below control level. For lung tissue, priming increased the amounts of PC and disaturated PC (DSPC) whereas terbutaline in vitro decreased DSPC in both primed and non-primed lungs. Terbutaline in vitro slightly increased the incorporation of 14C-choline and 3H-palmitate into PC and DSPC in non-primed but not in primed lungs. beta-adrenergic blockade by ICI 118.551 prevented all effects but generally increased 3H-palmitate incorporation into the phospholipids and, in lavagable cells, the amount of PC. We conclude that long-term beta-adrenergic treatment may alter the metabolism of pulmonary surfactant phospholipids by increasing tissue PC and DSPC and by decreasing the secretion of newly-synthesized PC.