Surfactant alterations in severe pneumonia, acute respiratory distress syndrome, and cardiogenic lung edema.
Surfactant alterations in severe pneumonia, acute respiratory distress syndrome, and cardiogenic lung edema.
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DOI：
10.1164/ajrccm.153.1.8542113
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发表时间：
1996
影响因子：
24.7
通讯作者：
A. Günther;C. Siebert;R. Schmidt;S. Ziegler;F. Grimminger;M. Yabut;B. Temmesfeld;D. Walmrath;H. Morr;W. Seeger
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文献类型：
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作者：
A. Günther;C. Siebert;R. Schmidt;S. Ziegler;F. Grimminger;M. Yabut;B. Temmesfeld;D. Walmrath;H. Morr;W. Seeger
分析了153例需要机械通气的急性呼吸衰竭患者支气管肺泡灌洗液（BALF）中的表面活性物质异常。诊断为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和PNEU（n = 36）和心源性肺水肿（CLE; n = 13）。PNEU组又分为肺泡PNEU组（n = 35）、支气管PNEU组（n = 16）、间质PNEU组（n = 18）和未分类PNEU组（n = 19）。与健康对照组（n = 20）进行比较。在原始BALF中定量总磷脂（PL）、蛋白质、PL类（HPTLC）和表面活性剂脱辅基蛋白SP-A和SP-B（ELISA）。使用来自BAL离心的48，000 x g沉淀来评估大表面活性剂聚集体（LSA）的百分比和表面活性剂的生物物理性质（脉动气泡表面活性计）。所有炎症性肺损伤（PNEU和/或ARDS）组的可灌洗PL池有所减少，BALF中LSA含量降低，肺泡蛋白负荷增加。在各组中均观察到PL特征的显著变化（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浓度降低，但SP-B浓度未降低。在对照组中，最小表面张力值接近0 mN/m，在不存在上清液蛋白的情况下，最小表面张力值范围为10至25 mN/m，在ARDS和/或PNEU组中，在与泄漏蛋白重组的情况下，最小表面张力值范围为20至35 mN/m。肺泡PNEU的代谢率明显高于支气管PNEU，间质PNEU的代谢变化明显。除了蛋白质对表面活性的轻微抑制外，CLE中不存在所有表面活性剂的变化。我们的结论是，明显的表面活性物质异常，在ARDS中的肺部感染的情况下，发生在不同的实体严重PNEU，但不是在CLE。
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.