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β ‐adrenergic priming of rats in vivo modulates the effect of β ‐agonist in vitro on surfactant phospholipid metabolism of isolated lungs
Author(s) -
BERNHARD W.,
MÜLLER B.,
WICHERT P. VON
Publication year - 1994
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1994.tb02182.x
Subject(s) - terbutaline , phospholipid , phosphatidylcholine , in vivo , priming (agriculture) , pulmonary surfactant , in vitro , endocrinology , chemistry , medicine , choline , adrenergic agonist , agonist , biology , biochemistry , receptor , botany , germination , microbiology and biotechnology , membrane , asthma
Abstract. To evaluate the effects of multiple β ‐adrenergic stimulations on pulmonary surfactant phospholipids, perfused lungs from β ‐adrenergic primed and non‐primed rats were challenged with the β ‐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 14 C‐choline and 3 H‐palmitate into total phosphatidylcholine (PC) and of 3 H‐palmitate into phosphatidylglycerol (PG). β ‐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 3 H‐palmitate into PC. Priming in vivo reduced this effect and diminished the specific 3 H‐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 14 C‐choline and 3 H‐palmitate into PC and DSPC in non‐primed but not in primed lungs. β ‐adrenergic blockade by ICI 118.551 prevented all effects but generally increased 3 H‐palmitate incorporation into the phospholipids and, in lavagable cells, the amount of PC. We conclude that long‐term β ‐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.