Reflections on the Introduction of Surfactant Therapy for Neonates with Respiratory Distress.

When pulmonary surfactant was first detected in the 1950s by Pattle and Clements, many thousands of infants perished each year due to a respiratory illness termed Hyaline Membrane Disease. Hyaline membranes are formed by plasma leaking through damaged endothelial barriers into the terminal bronchiolar: alveolar spaces. Since the leaking plasma lacks erythrocytes, these clots are opaque.

Impact of aging on pulmonary cellular responses during mechanical ventilation.

Acute respiratory distress syndrome (ARDS) results in significant morbidity and mortality, especially in the elderly. Mechanical ventilation, a common supportive treatment for ARDS, is necessary for maintaining gas exchange, but can also propagate injury. We hypothesized that aging leads to alterations in surfactant function, inflammatory signaling, and microvascular permeability within the lung during mechanical ventilation.

Alveolar epithelial glycocalyx degradation mediates surfactant dysfunction and contributes to acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure yet has few pharmacologic therapies, reflecting the mechanistic heterogeneity of lung injury. We hypothesized that damage to the alveolar epithelial glycocalyx, a layer of glycosaminoglycans interposed between the epithelium and surfactant, contributes to lung injury in patients with ARDS. Using mass spectrometry of airspace fluid noninvasively collected from mechanically ventilated patients, we found that airspace glycosaminoglycan shedding (an index of glycocalyx degradation) occurred predominantly in patients with direct lung injury and was associated with duration of mechanical ventilation.