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Evidence of lung surfactant abnormality in respiratory failure broncho alveolar lavage phospho lipids surface activity phospho lipase activity and plasma myo inositol

, : Evidence of lung surfactant abnormality in respiratory failure broncho alveolar lavage phospho lipids surface activity phospho lipase activity and plasma myo inositol. Journal of Clinical Investigation 70(3): 673-683

Lung surfactant is damaged in the adult respiratory distress syndrome. Bronchoalveolar lavage specimens (225: 78 from 36 patients 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease and 12 from healthy controls) were assayed for the lung profile [lecithin/sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol and phosphatidylglycerol]. Bronchoalveolar lavage fluid was analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2 and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity and plasma was measured for myoinositol. There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. In respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the L/S ratio, phosphatidylglycerol and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure and tended to normalize during recovery. Low L/S ratio (< 2) and low phosphatidylglycerol (1% or less of glycerophospholipids) in bronchoalveolar lavage was always associated with respiratory failure. Abnormal lavage phospholipids were not due to plasma contamination. The phospholipase studies revealed little evidence of increased catabolism of phospholipids. In respiratory failure, the lipid-protein complexes from lung lavage were not surface active, whereas that from healthy controls had surface properties similar to lung surfactant. Phospholipids from patients with respiratory failure were similar to those from respiratory distress syndrome in the newborn. The latter condition was characterized by fast recovery of surfactant deficiency and by high plasma myoinositol that suppressed the synthesis of surfactant phosphatidylglycerol and increased phosphatidylinositol. In adult respiratory distress syndrome, the abnormality in surfactant phospholipids may last for weeks and in most cases is associated with low phosphatidylinositol, low phosphatidylglycerol and low plasma myoinositol.

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