Lung phospholipids during recovery from oxygen toxicity are altered by hydrocortisone

Corticosteroids affect type II alveolar epithelial cells, increase the lung's content of lipids associated with pulmonary surfactant, and have been used to treat the adult respiratory distress syndrome. We used hyperoxia to produce diffuse alveolar damage in rats and then determined the contents of lung lipids and the incorporation of precursors into these lipids while the rats recovered in air and received either hydrocortisone or saline injections. With saline injections (control) the total lipid content after hyperoxia and 48 hours recovery in air was nearly twice the lipid content of lungs never exposed to hyperoxia; many lipids, including phosphatidylcholine (PC), shared in this increase. With hydrocortisone injections the total lipid content, when expressed per lung, was not significantly greater than with saline injections but when expressed per mg DNA several lipid subgroups, including phosphatidylcholine, were significantly greater. Palmitate incorporation into most lipids of lung slices was not significantly different by 48 hours of recovery, and hydrocortisone had a modest effect after 96 hours. In contrast to the incorporation of palmitate, the incorporation of glycerol and of lysophosphatidylcholine (LPC) nearly doubled in most lipids during the recovery phase. Hydrocortisone injections were associated with greater glycerol incorporation after 96 hours of recovery in nearly all lipids and LPC incorporation was increased primarily into PC. We conclude that lung lipids increase markedly during recovery from severe oxygen toxicity and that hydrocortisone leads to additional increases of saturated and unsaturated PC.