Günther A, Siebert C, Schmidt R, Ziegler S, Grimminger F, Yabut M, Temmesfeld B, Walmrath D, Morr H, Seeger W
Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany.
Am J Respir Crit Care Med. 1996 Jan;153(1):176-84. doi: 10.1164/ajrccm.153.1.8542113.
Bronchoalveolar lavage fluids (BALF) were analyzed for surfactant abnormalities in 153 patients with acute respiratory failure necessitating mechanical ventilation. Diagnoses were acute respiratory distress syndrome (ARDS) in the absence of lung infection (n = 16), severe pneumonia (PNEU; n = 88), ARDS and PNEU (n = 36), and cardiogenic lung edema (CLE; n = 13). The PNEU group was subdivided into groups with alveolar PNEU (n = 35), bronchial PNEU (n = 16), interstitial PNEU (n = 18) and nonclassified PNEU (n = 19). Comparison with healthy controls (n = 20) was undertaken. Total phospholipids (PL), proteins, PL classes (HPTLC) and surfactant apoproteins SP-A and SP-B (ELISA) were quantified in the original BALF. The 48,000 x g pellet from centrifugation of the BAL was used to assess the percentage of large surfactant aggregates (LSA) and the biophysical properties of the surfactant (pulsating bubble surfactometer). All groups with inflammatory lung injury (PNEU and/or ARDS) showed some decrease in the lavageable PL pool, a reduced LSA content in BALF, and a manifold increase in alveolar protein load. Marked changes in the PL profile were noted throughout the groups (a decrease in phosphatidylcholine (PC) and phosphatidylglycerol (PG) and an increase in phosphatidylinositol [PI] and sphingomyelin [SPH]). Concentrations of SP-A but not of SP-B in BALF were reduced. Minimum surface-tension values approached 0 mN/m in controls, and ranged from 10 to 25 mN/m in the absence of supernatant protein and from 20 to 35 mN/m in recombination with leaked protein in the groups with ARDS and/or PNEU. Abnormalities in alveolar PNEU surpassed those in bronchial PNEU, and interstitial PNEU presented a distinct pattern with extensive metabolic changes. All surfactant changes were absent in CLE except for a slight inhibition of surface activity by proteins. We conclude that pronounced surfactant abnormalities, comparable to those in ARDS in the absence of lung infection, occur in different entities of severe PNEU, but not in CLE.
对153例因急性呼吸衰竭需要机械通气的患者的支气管肺泡灌洗（BAL）液进行分析，以检测表面活性剂异常情况。诊断包括无肺部感染的急性呼吸窘迫综合征（ARDS，n = 16）、重症肺炎（PNEU，n = 88）、ARDS合并PNEU（n = 36）以及心源性肺水肿（CLE，n = 13）。PNEU组又细分为肺泡性PNEU组（n = 35）、支气管性PNEU组（n = 16）、间质性PNEU组（n = 18）和未分类PNEU组（n = 19）。与健康对照者（n = 20）进行了比较。对原始BALF中的总磷脂（PL）、蛋白质、PL类别（高效薄层层析法）以及表面活性剂载脂蛋白SP - A和SP - B（酶联免疫吸附测定法）进行了定量分析。BAL离心得到的48,000×g沉淀用于评估大表面活性剂聚集体（LSA）的百分比以及表面活性剂的生物物理特性（脉动气泡表面活性剂测定仪）。所有伴有炎性肺损伤的组（PNEU和/或ARDS）均显示可灌洗的PL池有所减少，BALF中LSA含量降低，肺泡蛋白负荷显著增加。所有组的PL谱均有明显变化（磷脂酰胆碱（PC）和磷脂酰甘油（PG）减少，磷脂酰肌醇（PI）和鞘磷脂（SPH）增加）。BALF中SP - A的浓度降低，但SP - B的浓度未降低。对照组的最小表面张力值接近0 mN/m，在ARDS和/或PNEU组中，无上清液蛋白时其范围为10至25 mN/m，与漏出蛋白重组后为20至35 mN/m。肺泡性PNEU的异常超过支气管性PNEU，间质性PNEU呈现出具有广泛代谢变化的独特模式。除了蛋白质对表面活性有轻微抑制外，CLE中不存在所有表面活性剂异常情况。我们得出结论，在严重PNEU的不同类型中会出现与无肺部感染的ARDS中类似的明显表面活性剂异常，但CLE中不会出现。
