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Recombinant thrombomodulin and recombinant antithrombin attenuate pulmonary endothelial glycocalyx degradation and neutrophil extracellular trap formation in ventilator-induced lung injury in the context of endotoxemia.
Respir Res
September 2024
Department of Anesthesiology, School of Medicine, Sapporo Medical University, S-1, W-16 Chuo-ku, Sapporo, 060-8543, Hokkaido, Japan.
Background: Vascular endothelial damage is involved in the development and exacerbation of ventilator-induced lung injury (VILI). Pulmonary endothelial glycocalyx and neutrophil extracellular traps (NETs) are endothelial protective and damaging factors, respectively; however, their dynamics in VILI and the effects of recombinant thrombomodulin and antithrombin on these dynamics remain unclear. We hypothesized that glycocalyx degradation and NETs are induced by VILI and suppressed by recombinant thrombomodulin, recombinant antithrombin, or their combination.
View Article and Find Full Text PDFBackground: Mechanical ventilation is a life-saving therapy for critically ill patients, providing rest to the respiratory muscles and facilitating gas exchange in the lungs. Ventilator-induced lung injury (VILI) is an unfortunate side effect of mechanical ventilation that may lead to serious consequences for the patient and increase mortality. The four main injury mechanisms associated with VILI are: baro/volutrauma caused by overstretching the lung tissues; atelectrauma, caused by repeated opening and closing of the alveoli resulting in shear stress; oxygen toxicity due to use of high ratio of oxygen in inspired air, causing formation of free radicals; and biotrauma, the resulting biological response to tissue injury, that leads to a cascade of events due to excessive inflammatory reactions and may cause multi-organ failure.
View Article and Find Full Text PDFIf We Ask a Mouse about Biotrauma, Will It Give Us a Sensible Answer?
Anesthesiology
May 2017
From the Section of Anaesthetics, Pain Medicine and Intensive Care, Faculty of Medicine, Imperial College London, London, United Kingdom.
One-hit Models of Ventilator-induced Lung Injury: Benign Inflammation versus Inflammation as a By-product.
Anesthesiology
May 2017
From the Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen University, Institute of Pharmacology and Toxicology, Aachen, Germany.
Background: One important explanation for the detrimental effects of conventional mechanical ventilation is the biotrauma hypothesis that ventilation may trigger proinflammatory responses that subsequently cause lung injury. This hypothesis has frequently been studied in so-called one-hit models (overventilation of healthy lungs) that so far have failed to establish an unequivocal link between inflammation and hypoxemic lung failure. This study was designed to develop a one-hit biotrauma model.
View Article and Find Full Text PDFObjectives: Many mechanically ventilated patients with acute respiratory distress syndrome develop pulmonary fibrosis. Stresses induced by mechanical ventilation may explain the development of fibrosis by a number of mechanisms (e.g.
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