Effects of breathing 80% oxygen on water and albumin accumulation in oleic acid-injured rabbit lungs.

This study was done to determine whether breathing 80% oxygen would enhance edema formation in oleic acid (OA) lung injury. Rabbits breathed air (n = 51) or 80% oxygen (n = 51) for 1 to 7 days after OA lung injury (0.09 ml/kg iv). Control groups breathed 80% oxygen (n = 37) or room air (n = 8) without OA injury. Pulmonary vascular permeability was assessed by measuring 131I-albumin (RISA) concentration in extravascular, extracellular lung water (EVECW) relative to plasma (RISAL/RISAPL). EVECW (ml/g dry lung) was measured by 24Na, and total lung water (TLW) by wet/dry weight (g/g dry lung). Air-breathing control values were 4.53 +/- 0.25 (SD) for TLW and 0.40 +/- 0.09 for RISAL/RISAPL. In the air-breathing OA group, TLW and RISAL/RISAPL increased to 8.32 +/- 0.85 and 0.93 +/- 0.16, respectively, 2 h after OA (p less than .001) but by 24 h, were equal to air-breathing controls. TLW and RISAL/RISAPL in the oxygen treated OA group did not differ from the air breathing OA group on days 2 through 7 inclusive, suggesting that 80% oxygen had no effect on edema formation in the OA-injured lung. Breathing 80% oxygen alone, without OA injury, significantly (p less than .005) increased TLW and RISAL/RISAPL on days 5 and 6. Thus, preexisting lung injury had a protective effect against edema formation from a high fraction of inspired oxygen.