In vitro study also showed that IL-6 increased the permeability of pulmonary endothelial cells in a Rho-independent manner. Intratracheal administration of IL-6 itself increased cell count and protein concentration in the BALF, while high V T MV further increased lung permeability following IL-6 administration in mice. The decreased IL-6 levels and reduced VILI in IKKβ Δmye mice suggested that NF-κB activation-induced IL-6 expression may contribute to VILI. A significant decrease in ventilation-induced IL-6 levels in the lung and BALF was observed in IKKβ Δmye mice compared to WT mice while left IL-1β unaffected. ![]() ![]() Among these, the levels of IL-6 and IL-1β in the lung and BALF of IKKβ Δmye mice were also found to cause nuclear factor-κB (NF-κB) activation in ventilator-induced IL-6 and IL-1β production. High V T ventilation increases interleukin (IL)-1β, IL-6, IL-8, tumor-necrosis factor (TNF)-α, C-X-C motif ligand 1 (CXCL1) and CXCL10, macrophage inflammatory protein (MIP)-2, and intercellular cell adhesion molecule levels in the bronchoalveolar lavage fluid (BALF) in mice with a significant increase in pulmonary vascular permeability. MV is able to trigger the release of numerous proinflammatory mediators that may induce lung injury and impair pulmonary function. Accumulating evidence showed that biotrauma induced by MV is far more complicated than barotrauma, volutrauma, or atelectrauma and the underlying mechanisms can be categorized in the following four parts. Since then, more attention has been paid to how MV triggers biotrauma within the lung. The study of Slutsky and Tremblay first suggested that the MV-induced inflammatory response may contribute to the development of multiple system organ dysfunction including respiratory failure in mechanically ventilated patients with ARDS. In certain circumstances, MV is able to initiate inflammation and lung injury while maintain gas exchange. ![]() The role of biotrauma in the pathogenesis of VILI was not clarified until 1998. This review addressed several core mechanisms underlying VILI. An integrated understanding of the molecular pathways regarding VILI is the foundation of choosing the right strategy of MV, which certainly will help clinicians to make decisions in their daily work. Guidelines for clinical practices are needed when it comes to how to ventilate the critical illness with or without ARDS, such as whether or not to apply low tidal volume (V T) ventilation. Ideally, MV should maintain lung units open throughout the ventilator cycle, which minimizes lung injury due to repetitive alveolar collapse and/or overdistention. To understand the mechanisms of VILI are one thing, to apply MV and avoid VILI are another. Indeed, the concept of VILI has been shifted from conventional barotraumas/volutrauma/atelectrauma to modernized biotrauma, in which the inflammatory mediators were found to be responsible for the onset of VILI. Gradually, clinicians realized that MV also mediated pulmonary injury without causing volutrauma or atelectrauma, even multi-organ dysfunction syndrome, and systemic inflammatory response. Mechanical ventilation (MV) is essential life support for patients with acute respiratory distress syndrome (ARDS) however, it can also lead to ventilator-induced lung injury (VILI) due to regional alveolar overstretch and/or repetitive alveolar collapse, which were termed as barotrauma, volutrauma, and atelectrauma.
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