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Updated: Aug 21, 2026

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
Published on: April 7, 2021
Dysfunction of pulmonary surfactant in chronically ventilated premature infants
Jeffrey D Merrill1, Roberta A Ballard, Avital Cnaan
1Neonatology, Department of Pediatrics, University of Pennsylvania School of Medicine, USA.
Insights
Most premature infants needing respiratory support develop abnormal surfactant function due to deficiencies in surfactant proteins SP-B and SP-C. This dysfunction is linked to infection and respiratory decline, impacting long-term pulmonary health.
Area of Science:
- Neonatal Medicine
- Respiratory Physiology
- Biochemistry
Background:
- Premature infants (<30 wk gestation) often require prolonged respiratory support.
- Bronchopulmonary dysplasia (BPD) is a significant risk in these infants, leading to long-term pulmonary issues or death.
- Surfactant dysfunction is implicated in respiratory distress.
Purpose of the Study:
- To investigate surfactant status in premature infants at high risk for BPD.
- To identify factors associated with abnormal surfactant function in this population.
Main Methods:
- Prospective analysis of 247 tracheal aspirate samples from 68 infants (23-30 wk gestation) intubated for 7-84 days.
- Surfactant function assessed using a pulsating bubble surfactometer (minimum surface tension).
- Surfactant protein (SP) A, B, and C levels measured by immunoassay in surfactant pellets.
Main Results:
- 75% of infants exhibited abnormal surfactant function (elevated minimum surface tension).
- Abnormal surfactant function correlated with infection (p=0.01) and respiratory deterioration (p=0.005).
- Reduced levels of SP-A (50%), SP-B (80%), and SP-C (72%) were found in samples with abnormal surface tension. SP-B and SP-C content strongly correlated with surfactant function (p<0.0001).
Conclusions:
- Premature infants requiring prolonged respiratory support frequently experience transient surfactant dysfunction.
- This dysfunction is characterized by deficiencies in surfactant proteins SP-B and SP-C.
- Surfactant protein deficiencies are linked to clinical events like infection and respiratory decline in high-risk infants.
Abstract:
Infants of <30 wk gestation often require respiratory support for several weeks and may develop bronchopulmonary dysplasia (BPD), which is associated with long-term pulmonary disability or death in severe cases. To examine the status of surfactant in infants at high risk for BPD, this prospective study analyzed 247 tracheal aspirate samples from 68 infants of 23-30 wk gestation who remained intubated for 7-84 d. Seventy-five percent of the infants had one or more surfactant samples with abnormal function (minimum surface tension 5.1-21.7 mN/m by pulsating bubble surfactometer), which were temporally associated with episodes of infection (p = 0.01) and respiratory deterioration (p = 0.005). Comparing normal and abnormal surfactant samples, there were no differences in amount of surfactant phospholipid, normalized to total protein that was recovered from tracheal aspirate, or in relative content of phosphatidylcholine and phosphatidylglycerol. Contents of surfactant proteins (SP) A, B, and C, measured in the surfactant pellet by immunoassay, were reduced by 50%, 80%, and 72%, respectively, in samples with abnormal surface tension (p < or = 0.001). On multivariable analysis of all samples, SP-B content (r = -0.58, p < 0.0001) and SP-C content (r = -0.32, p < 0.001) were correlated with surfactant function. We conclude that most premature infants requiring continued respiratory support after 7 d of age experience transient episodes of dysfunctional surfactant that are associated with a deficiency of SP-B and SP-C.
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