Abstract
Mechanical ventilation is a supportive therapy for patients with acute respiratory distress syndrome (ARDS). However, it also inevitably produces or aggravates the original lung injury with pathophysiological changes of pulmonary edema caused by increased permeability of alveolar capillaries which composed of microvascular endothelium, alveolar epithelium, and basement membrane. Vascular endothelium forms a semi-selective barrier to regulate body fluid balance. Mechanical ventilation in critically ill patients produces a mechanical force on lung vascular endothelium when the endothelial barrier was destructed. This review aims to provide a comprehensive overview of molecular and signaling mechanisms underlying the endothelial barrier permeability in ventilator-induced lung jury (VILI).
Highlights
Acute respiratory distress syndrome (ARDS) is a condition in which lungs sustain an acute, diffuse, and inflammatory injury (Force et al, 2012; Fan et al, 2018)
Integrin β8 has a non-classical cytoplasmic domain and plays a role in angiogenesis integrin β6 is principally expressed in epithelium and play an Platelet-endothelial cell adhesion molecule 1 (PECAM-1), a member of immunoglobulin superfamily cell adhesion molecules (IgCAMs) family, is located at ECs intercellular junctions, where it functions as a mechanosensor and maintenance of ECs junctional integrity (Privratsky and Newman, 2014; Liao et al, 2018)
Hoetzel found that ventilation with 12 ml/kg for 8 h increased Cav-1 expression levels, and Cav-1 deficiency aggravated lung injury characterized by protein leakage, edema formation, and macrophage infiltration, suggesting that Cav-1−/− mice were more susceptible to pulmonary endothelial hyperpermeability induced by mechanical ventilation (Hoetzel et al, 2009)
Summary
Acute respiratory distress syndrome (ARDS) is a condition in which lungs sustain an acute, diffuse, and inflammatory injury (Force et al, 2012; Fan et al, 2018). Mechanical ventilation inevitably damages or aggravates the original lung injury characterized by inflammatory-cell infiltrates, formation of hyaline membranes, increased vascular permeability, and pulmonary edema (Slutsky and Ranieri, 2013). Exploring the mechanisms of endothelial layer responding to mechanical force is vital to develop effective endothelial-targeted treatments among patients who require mechanical ventilation. The primary purposes of this review are to (1) illustrate the increase of pulmonary microvascular endothelial permeability induced by mechanical ventilation, (2) summarize the destruction of endothelial barrier function caused by mechanical force, and 3) describe the molecular mechanisms involved in endothelial barrier disfunction
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