EVIDENCE OF LUNG SURFACTANT ABNORMALITY IN RESPIRATORY-FAILURE - STUDY OF BRONCHOALVEOLAR LAVAGE PHOSPHOLIPIDS, SURFACE-ACTIVITY, PHOSPHOLIPASE-ACTIVITY, AND PLASMA MYOINOSITOL
EVIDENCE OF LUNG SURFACTANT ABNORMALITY IN RESPIRATORY-FAILURE - STUDY OF BRONCHOALVEOLAR LAVAGE PHOSPHOLIPIDS, SURFACE-ACTIVITY, PHOSPHOLIPASE-ACTIVITY, AND PLASMA MYOINOSITOL
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DOI：
10.1172/jci110662
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发表时间：
1982-01-01
影响因子：
15.9
通讯作者：
GLUCK, L
中科院分区：
文献类型：
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作者：
HALLMAN, M;SPRAGG, R;GLUCK, L
肺表面活性物质在成人呼吸窘迫综合征中受损。对支气管肺泡灌洗标本（225：78份来自36例1-78岁呼吸衰竭患者，135份来自另外128例其他呼吸系统疾病患者，12份来自健康对照）进行肺特征分析[卵磷脂/鞘磷脂（L/S）比、饱和卵磷脂、磷脂酰肌醇和磷脂酰甘油]。分析支气管肺泡灌洗液中的磷脂和磷脂酸磷酸水解酶、磷脂酶A2和磷脂酰肌醇磷酸二酯酶活性。分离脂质-蛋白质复合物并分析其表面活性，并测量血浆中的肌醇。呼吸衰竭患者和正常对照组之间的总磷脂回收率只有很小的差异。在呼吸衰竭中，支气管肺泡灌洗液中的磷脂质与正常对照组或其他肺部疾病患者中的磷脂质有质的不同：L/S比、磷脂酰甘油和二饱和卵磷脂较低，而鞘磷脂和磷脂酰丝氨酸则很突出。这些异常在呼吸衰竭早期出现，并在恢复期间趋于正常。支气管肺泡灌洗液中低L/S比值（< 2）和低磷脂酰甘油（甘油磷脂的1%或更少）总是与呼吸衰竭相关。灌洗液磷脂异常不是由于血浆污染。磷脂酶的研究表明，几乎没有证据表明磷脂的催化活性增加。在呼吸衰竭中，肺灌洗液中的脂质-蛋白质复合物不具有表面活性，而健康对照组的脂质-蛋白质复合物具有与肺表面活性物质相似的表面性质。呼吸衰竭患者的磷脂与新生儿呼吸窘迫综合征的磷脂相似。后一种情况的特点是表面活性剂缺乏症的快速恢复和高血浆肌醇抑制表面活性剂磷脂酰甘油的合成和增加磷脂酰肌醇。在成人呼吸窘迫综合征中，表面活性磷脂的异常可持续数周，在大多数情况下与低磷脂酰肌醇、低磷脂酰甘油和低血浆肌醇有关。
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.