scholarly journals Acute Respiratory Distress Syndrome: Insights Gained from Clinical and Translational Research

2009 ◽  
Vol 9 (1) ◽  
pp. S59-S68 ◽  
Author(s):  
Marija Kojicic ◽  
Emir Festic ◽  
Ognjen Gajic
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Severe Form ◽  
Ventilator Induced Lung Injury ◽  
Protective Mechanical Ventilation ◽  
Lung Protective Mechanical Ventilation

Acute lung injury and its more severe form acute respiratory distress syndrome (ARDS) are characterized by diffuse impairment of alveolocapillary membrane in the settings of different predisposing conditions such as sepsis, trauma and shock. Many intrahospital exposures, including aspiration, delayed resuscitation, high tidal volume mechanical ventilation and non critical use of transfusions may contribute or worsen ARDS. Therapy is targeted to treatment of predisposing condition, life supportive measures and prevention of nosocomial complications. Rigorous adherence to lung-protective mechanical ventilation is critical to prevent ventilator induced lung injury and decrease mortality. Although survival of ARDS patients has improved in the last decades ARDS mortality rates are still high and survivors encounter significant physical and psychological impairments

scholarly journals Mechanosensitive activation of mTORC1 mediates ventilator induced lung injury during the acute respiratory distress syndrome

2020 ◽  
Author(s):  
Hyunwook Lee ◽  
Qinqin Fei ◽  
Adam Streicher ◽  
Wenjuan Zhang ◽  
Colleen Isabelle ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Lung Epithelial Cells ◽  
Ventilator Induced Lung Injury ◽  
Lung Epithelial

AbstractAcute respiratory distress syndrome (ARDS) is a highly lethal condition that impairs lung function and causes respiratory failure. Mechanical ventilation maintains gas exchange in patients with ARDS, but exposes lung cells to physical forces that exacerbate lung injury. Our data demonstrate that mTOR complex 1 (mTORC1) is a mechanosensor in lung epithelial cells and that activation of this pathway during mechanical ventilation exacerbates lung injury. We found that mTORC1 is activated in lung epithelial cells following volutrauma and atelectrauma in mice and humanized in vitro models of the lung microenvironment. mTORC1 is also activated in lung tissue of mechanically ventilated patients with ARDS. Deletion of Tsc2, a negative regulator of mTORC1, in epithelial cells exacerbates physiologic lung dysfunction during mechanical ventilation. Conversely, treatment with rapamycin at the time mechanical ventilation is initiated prevents physiologic lung injury (i.e. decreased compliance) without altering lung inflammation or barrier permeability. mTORC1 inhibition mitigates physiologic lung injury by preventing surfactant dysfunction during mechanical ventilation. Our data demonstrate that in contrast to canonical mTORC1 activation under favorable growth conditions, activation of mTORC1 during mechanical ventilation exacerbates lung injury and inhibition of this pathway may be a novel therapeutic target to mitigate ventilator induced lung injury during ARDS.

scholarly journals Desflurane Attenuates Ventilator-Induced Lung Injury in Rats with Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xue Lin ◽  
Ying-nan Ju ◽  
Wei Gao ◽  
Dong-mei Li ◽  
Chang-chun Guo
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Tidal Volume ◽  
Lung Tissue ◽  
Rat Model ◽  
Distress Syndrome ◽  
Inflammatory Factors ◽  
Ventilator Induced Lung Injury

Ventilator-induced lung injury aggravates the existing lung injury. This study investigated the effect of desflurane on VILI in a rat model of acute respiratory distress syndrome. Forty-eight rats were randomized into a sham (S) group, control (C) group, lipopolysaccharide/ventilation (LV) group, lipopolysaccharide/ventilation/desflurane (LVD) group, or lipopolysaccharide/low ventilation with and without desflurane (LLV and LLVD) groups. Rats in the S group received anesthesia only. Rats in the LV and LVD groups received lipopolysaccharide and were ventilated with a high tidal volume. Rats in LLV and LLVD groups were treated as the LV and LVD groups and ventilated with a low tidal volume. PaO2/FiO2, lung wet-to-dry weight ratios, concentrations of inflammatory factors in serum and BALF, histopathologic analysis of lung tissue, and levels of nuclear factor- (NF-) κB protein in lung tissue were investigated. PaO2/FiO2 was significantly increased by desflurane. Total cell count, macrophages, and neutrophils in BALF and proinflammatory factors in BALF and serum were significantly decreased by desflurane, while IL-10 was increased. The histopathological changes and levels of NF-κB protein in lung tissue were decreased by desflurane. The results indicated that desflurane ameliorated VILI in a rat model of acute respiratory distress syndrome.

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