![]() ![]() Respiratory rate (RR) ( Rich et al., 2003) as well as inspiratory ( Fujita et al., 2007) and expiratory ( Schumann et al., 2014) airflow have also been implicated in VILI. Additionally, the respiratory system driving pressure (ΔP, RS) is associated with increased lung inflammation ( Bellani et al., 2011) and predicts mortality rate in ARDS ( Amato et al., 2015). In patients with the acute respiratory distress syndrome (ARDS), V T level has been recognized as a major risk factor for organ failure and death ( Brower et al., 2000 Putensen et al., 2009), and the use of low V T (4–8 mL/kg) represents the cornerstone of protective mechanical ventilation ( Bellani et al., 2016 Fan et al., 2017). Mechanical ventilation with high tidal volume (V T) can promote ventilator-induced lung injury (VILI) ( Tremblay and Slutsky, 2006). V T control seems to be more important than RR control to mitigate VILI. In the model of ARDS used herein, even at low mechanical power, high V T resulted in VILI. Multiple linear regression analyses indicated that V T was able to predict changes in IL-6 and CC16, whereas ΔP, L predicted pHa, oxygenation, amphiregulin, and syndecan-1 expression. V T = 22 mL/kg was associated with higher IL-6, amphiregulin, CC16, MMP-9, and syndecan-1 mRNA expression and lower decorin expression than V T = 6 mL/kg. Accordingly, DAD score increased in V T = 22 mL/kg compared to V T = 6 mL/kg and V T = 13 mL/kg. ΔP, L and mechanical energy were higher in V T = 22 mL/kg than V T = 6 mL/kg and V T = 13 mL/kg ( p < 0.001 for both). Mechanical power was comparable among groups, while V T gradually increased. Seven rats were not mechanically ventilated (NV) and were used for molecular biology analysis. Mechanical power was calculated as × RR (ΔP, L = transpulmonary driving pressure, Est, L = static lung elastance). In the second and third groups, RR was adjusted to yield low mechanical power comparable to that of the first group. After 24 h, 21 animals were randomly assigned to ventilation (2 h) with low mechanical power at three different V T levels ( n = 7/group): (1) V T = 6 mL/kg and RR adjusted to normocapnia (2) V T = 13 mL/kg and 3) V T = 22 mL/kg. Twenty-eight Wistar rats received Escherichia coli lipopolysaccharide intratracheally. The present study aimed to investigate the impact of different V T levels and respiratory rates (RR) on lung function, diffuse alveolar damage (DAD), alveolar ultrastructure, and expression of genes related to inflammation, alveolar stretch (amphiregulin), epithelial and endothelial cell injury, and extracellular matrix damage in experimental acute respiratory distress syndrome (ARDS) under low-power mechanical ventilation. We hypothesized that, as long as mechanical power is kept below a safe threshold, high V T should not be injurious. Recently, experimental studies have suggested that mechanical power transferred from the ventilator to the lungs is the promoter of VILI. Tidal volume (V T) has been considered the main determinant of ventilator-induced lung injury (VILI).
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