Pison U, Obertacke U, Brand M, Seeger W, Joka T, Bruch J, Schmit-Neuerburg K P
University Clinic, Essen, Medical Faculty of the University of Essen, Department of Trauma Surgery, FRG.
J Trauma. 1990 Jan;30(1):19-26. doi: 10.1097/00005373-199001000-00003.
Pulmonary surfactant, which is crucial for alveolar stability, may also be involved in endogenous defense mechanisms of the lungs. Thus, alterations in pulmonary surfactant may promote infections, including pneumonia and septicemia. Because patients who have acute respiratory failure often develop pneumonia, thus septicemia, we investigated when surfactant is altered in these patients and whether there is a specific pattern of changes in surfactant phospholipid composition associated with septicemia in these patients. To answer these questions, we determined the phospholipid content and composition in lung washings obtained from alveolar sites (by bronchoalveolar lavage) and from tracheal sites (by aspiration). Both techniques were performed serially over a period of 18 days in 30 patients who had acute respiratory failure resulting from polytrauma, 18 of whom developed septicemia caused by pneumonia. We found that in lung washings obtained from the alveolar sites from all patients, the phosphatidylglycerol content was decreased and the phosphatidylinositol content was increased as early as 6 hr after trauma and normalized during recovery of the patients. In addition, alveolar phosphatidylcholine content was decreased 24 hr after trauma. In patients who developed septicemia during the observation time, but not in patients who had uncomplicated courses of acute respiratory failure, the concentrations of alveolar phosphatidylethanolamine (normally 4.8% of total phospholipids) and alveolar phosphatidylcholine (normally 62.8%) both approached the proportions found in the trachea (phosphatidylethanolamine 33.4%, phosphatidylcholine 35.6%), suggesting that surfactant phospholipid pool size had progressively decreased. Our results indicate that in patients who have acute respiratory failure, pulmonary surfactant is altered very early, and that when septicemia complicates the course of acute respiratory failure, the surfactant phospholipid pool size decreases progressively.(ABSTRACT TRUNCATED AT 250 WORDS)
对肺泡稳定性至关重要的肺表面活性物质，可能也参与了肺的内源性防御机制。因此，肺表面活性物质的改变可能会促进感染，包括肺炎和败血症。由于急性呼吸衰竭患者常并发肺炎，进而引发败血症，我们研究了这些患者何时出现表面活性物质改变，以及这些患者中与败血症相关的表面活性物质磷脂组成是否存在特定的变化模式。为回答这些问题，我们测定了从肺泡部位（通过支气管肺泡灌洗）和气管部位（通过抽吸）获取的肺灌洗液中的磷脂含量和组成。在30例因多发伤导致急性呼吸衰竭的患者中，这两种技术在18天内连续进行，其中18例因肺炎引发败血症。我们发现，在所有患者肺泡部位获取的肺灌洗液中，创伤后6小时磷脂酰甘油含量即下降，磷脂酰肌醇含量增加，且在患者恢复过程中恢复正常。此外，创伤后24小时肺泡磷脂酰胆碱含量下降。在观察期内发生败血症的患者中，但非急性呼吸衰竭病情未复杂发展的患者中，肺泡磷脂酰乙醇胺（正常情况下占总磷脂的4.8%）和肺泡磷脂酰胆碱（正常情况下占62.8%）的浓度均接近气管中的比例（磷脂酰乙醇胺33.4%，磷脂酰胆碱35.6%），表明表面活性物质磷脂池大小逐渐减小。我们的结果表明，急性呼吸衰竭患者的肺表面活性物质在早期即发生改变，且当败血症使急性呼吸衰竭病情复杂化时，表面活性物质磷脂池大小会逐渐减小。（摘要截选至250词）
