Influence of a beta-adrenergic agonist on septic shock-induced alterations of phosphatidylcholine metabolism in rat lung.

Changes in surfactant function play an important part in the pathogenesis of adult respiratory distress syndrome (ARDS). Since beta-adrenergic agonists have been shown to exert a decisive influence on surfactant secretion, we studied the effect of fenoterol on lung phospholipid metabolism under conditions of experimental sepsis. Fenoterol administered to live rats increased the incorporation of choline into lung tissue by 80% in normal, by 35% in septic animals. It had no comparable effect on palmitate incorporation. It increased the activity of choline kinase in control animals, but had no additional effect on animals with increased values due to sepsis. Phosphotransferase activity diminished during sepsis was stimulated, and phospholipase activity reduced. Fenoterol restored phosphatidylcholine to normal levels in lung tissue and bronchoalveolar lavage and prevented lysophosphatidylcholine generation. Fenoterol also increased the amount of palmitate in phosphatidylcholine from bronchoalveolar lavage in septic animals. The results imply that a beta-adrenergic agonist influences the conditions of lung phospholipid metabolism altered by sepsis towards normal.