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Updated: Oct 1, 2026

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
Published on: February 26, 2017
Protein content and biophysical properties of tracheal aspirates form neonates with respiratory failure
Eva Landmann1, L Gortner, I Reiss
1Pediatric Center, Justus-Liebig-University, Giessen, Germany. Eva.Landmann@paediat.med.uni-giessen.de
Background:
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.
Patients And Methods:
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.
Results:
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.
Conclusions:
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.
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