Stemming from the success in NRDS, it is widely believed that surfactant therapy should likewise reduce VILI in ARDS. In NRDS, surfactant therapy, i.e., tracheal instillation of exogenous surfactant, is a successful intervention that supplements the low surfactant level of immature lungs and reduces or prevents VILI ( Clements, 1997). Additionally, in ARDS, alveolar T is believed to be elevated ( Günther et al., 1996 Holm et al., 1999).īoth NRDS and ARDS patients are treated by mechanical ventilation, which supports gas exchange but also causes an exacerbation of underlying lung injury-known as ventilation-induced lung injury (VILI)-and can prevent patient recovery ( Jobe et al., 1983 Brower et al., 2000 Cereda et al., 2017). The edema liquid, which contains plasma proteins, impairs gas exchange. Barrier permeability leads first to interstitial and then to alveolar edema. In ARDS, regardless of initial insult, pulmonary inflammation is present and causes an increase in alveolar–capillary barrier permeability. In adults, a variety of pulmonary or systemic insults-e.g., pneumonia caused by a corona-virus, gastric aspiration, sepsis, or acute pancreatitis-can lead to acute respiratory distress syndrome (ARDS) ( Ware, 2006 Wu et al., 2020). This situation demonstrates the important contribution of T to lung mechanics. In neonatal respiratory distress syndrome (NRDS), babies born severely prematurely have reduced levels of lung surfactant, thus high surface tension in their lungs, and are unable to breathe unassisted ( Clements, 1997). Surfactant is first produced in the third trimester of gestation. Surfactant reduces T at the alveolar interface, yet T varies cyclically as lung inflation decreases interfacial surfactant concentration and increases T ( Kharge et al., 2014). The impact of T is lessened by alveolar epithelial type II cell secretion of pulmonary surfactant, a complex mixture of phospholipids, neutral lipids, and hydrophobic and hydrophilic proteins ( Haagsman and van Golde, 1991).
Surface tension acts in parallel with lung tissue elasticity to tend to collapse the lungs. In healthy lungs, the alveoli are lined by a thin, aqueous liquid lining layer with associated surface tension, T ( Gil et al., 1979).
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