Landmann Eva, Gortner L, Reiss I, Weller E, Tegtmeyer F K
Pediatric Center, Justus-Liebig-University, Giessen, Germany.
Klin Padiatr. 2002 Jan-Feb;214(1):1-7. doi: 10.1055/s-2002-19859.
We aimed at assessing the quality and quantity of protein-leakage across the alveolar-capillary membrane and its influence on surfactant function during the early neonatal period in preterm infants compared to newborns both with respiratory failure.
We therefore prospectively analyzed total protein, elastase-alpha1-proteinase inhibitor complex (E-alpha1-PI) and alpha2-macroglobulin concentrations in tracheal aspirates from 31 infants < or = 32 weeks gestational age (group 1 : 29.3 +/- 2 weeks, 1214 +/- 410 g [means +/- SEM]) and from 21 neonates > 32 weeks (group 2 : 37.5 +/- 3 weeks, 2890 +/- 600 g [means +/- SEM]) and measured their surface activity in the pulsating bubble surfactometer.
Day 1 total protein and alpha2-macroglobulin levels indicated an initial high leakage that declined to day 3 in both groups (from 1652 +/- 241 to 708 +/- 227 mg/l; p < 0.05; resp. from 28 +/- 6 to 12 +/- 4 mg/l [means +/- SEM]). In group 2 E-alpha1-PI concentrations were significantly elevated at day 1 compared to group 1 (15 754 +/- 5766 versus 3320 +/- 1056 microg/l [means +/- SEM]). In both groups a high minimum surface tension (15 - 30 mN/m) was recorded from day 1 - 4.
These results suggest in larger newborns a secondary surfactant deficiency due to protein-leakage to play an important role in the pathogenesis of respiratory failure. The increased alveolar-capillary membrane permeability might be caused by inflammatory ARDS-like mechanisms.
我们旨在评估与患有呼吸衰竭的新生儿相比,早产儿在新生儿早期经肺泡 - 毛细血管膜的蛋白质渗漏的质量和数量及其对表面活性物质功能的影响。
因此,我们前瞻性分析了31例胎龄≤32周婴儿(第1组:29.3±2周,1214±410克[均值±标准误])和21例胎龄>32周新生儿(第2组:37.5±3周,2890±600克[均值±标准误])气管吸出物中的总蛋白、弹性蛋白酶 - α1 - 蛋白酶抑制剂复合物(E - α1 - PI)和α2 - 巨球蛋白浓度,并在脉动气泡表面活性物质测定仪中测量其表面活性。
第1天的总蛋白和α2 - 巨球蛋白水平表明初始渗漏较高,两组在第3天均下降(从1652±241降至708±227毫克/升;p<0.05;分别从28±6降至12±4毫克/升[均值±标准误])。与第1组相比,第2组第1天的E - α1 - PI浓度显著升高(15754±5766对3320±1056微克/升[均值±标准误])。两组在第1 - 4天均记录到较高的最小表面张力(15 - 30毫牛顿/米)。
这些结果表明,在较大的新生儿中,由于蛋白质渗漏导致的继发性表面活性物质缺乏在呼吸衰竭的发病机制中起重要作用。肺泡 - 毛细血管膜通透性增加可能由类似炎症性ARDS的机制引起。