Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

2002 ◽  
Vol 103 (3) ◽  
pp. 284-295 ◽  
Author(s):  
Lucille London ◽  
Elizabeth I. Majeski ◽  
Sanja Altman-Hamamdzic ◽  
Candace Enockson ◽  
Manjeet K. Paintlia ◽  
...  
2016 ◽  
Vol 48 (6) ◽  
pp. 1794-1796 ◽  
Author(s):  
Colombe Saillard ◽  
Magali Bisbal ◽  
Antoine Sannini ◽  
Laurent Chow-Chine ◽  
Jean-Paul Brun ◽  
...  

2015 ◽  
Vol 41 (11) ◽  
pp. 1921-1930 ◽  
Author(s):  
José A. Lorente ◽  
Pablo Cardinal-Fernández ◽  
Diego Muñoz ◽  
Fernando Frutos-Vivar ◽  
Arnaud W. Thille ◽  
...  

1999 ◽  
Vol 6 (1) ◽  
pp. 71-86 ◽  
Author(s):  
Olivier Lesur ◽  
Yves Berthiaume ◽  
Gilbert Blaise ◽  
Pierre Damas ◽  
Éric Deland ◽  
...  

Acute respiratory distress syndrome (ARDS) was first described about 30 years ago. Modern definitions and statements have recently been proposed to describe ARDS accurately, but none is perfect. Diffuse alveolar damage is the basic pathological pattern most commonly observed in ARDS, and the term includes permeability edema. The alveolar epithelium of the alveolar-capillary barrier is clearly a key component requiring repair, given its multipotent functional activity. Lung inflammation and neutrophil accumulation are essential markers of disease in ARDS, and a wide variety of pro- and anti-inflammatory cytokines have been described in the alveolar fluid and blood of patients. These molecules still have to prove their value as diagnostic or prognostic biomarkers of ARDS.Supportive therapy in ARDS improved in the past decade; mechanical ventilation with lung protective strategies and patient positioning are gaining interest, but the indications for corticosteroids for ARDS are still debated. Nitric oxide may have a place in the treatment of one-third of patients. Novel approaches, such as surfactant replacement and liquid ventilation, may further improve supportive therapy. Innovative interventions may be on the horizon in treatments that help to resolve or modulate common pathways of ARDS, such as inflammation (eg, granulocyte-colony stimulating factor) or epithelial repair (eg, keratinocyte growth factor).


2021 ◽  
Author(s):  
Mohamad Hakam Tiba ◽  
Brendan M. McCracken ◽  
Danielle C. Leander ◽  
Carmen I. Colmenero ◽  
Jean A. Nemzek ◽  
...  

AbstractTo date, existing animal models of the acute respiratory distress syndrome (ARDS) have failed to translate preclinical discoveries into effective pharmacotherapy or diagnostic biomarkers. To address this translational gap, we developed a high-fidelity swine model of ARDS utilizing clinically-relevant lung injury exposures. Fourteen male swine were anesthetized, mechanically ventilated, and surgically instrumented for hemodynamic monitoring, blood, and tissue sampling. Animals were allocated to one of three groups: 1) Indirect lung injury only: animals were inoculated by direct injection of E. coli into the kidney parenchyma, provoking systemic inflammation and distributive shock physiology; 2) Direct lung injury only: animals received volutrauma, hyperoxia, and bronchoscope-delivered gastric particles; 3) Combined indirect and direct lung injury: animals were administered both above-described indirect and direct lung injury exposures. Animals were monitored for up to 12 hours, with serial collection of physiologic data, blood samples, and radiographic imaging. Lung tissue was acquired post-mortem for pathological examination. In contrast to indirect lung injury only and direct lung injury only groups, animals in the combined indirect and direct lung injury group exhibited all of the physiological, radiographic, and histopathologic hallmarks of human ARDS: impaired gas exchange (mean PaO2/FiO2 ratio 124.8 ± 63.8), diffuse bilateral opacities on chest radiographs, and extensive pathologic evidence of diffuse alveolar damage. Our novel porcine model of ARDS, built on clinically-relevant lung injury exposures, faithfully recapitulates the physiologic, radiographic, and histopathologic features of human ARDS, and fills a crucial gap in the translational study of human lung injury.


Biomeditsina ◽  
2020 ◽  
Vol 16 (4) ◽  
pp. 24-33
Author(s):  
I. A. Pomytkin ◽  
V. N. Karkischenko ◽  
Yu. V. Fokin ◽  
M. S. Nesterov ◽  
N. V. Petrova

This study was aimed at developing an experimental model of fatal acute lung injury and acute respiratory distress syndrome (ARDS) based on the intratracheal administration of bacterial lipopolysaccharide (LPS) in combination with muramylpeptide and Freund’s complete adjuvant to C57Bl/6Y mice sensitized with α-galactosylceramide. The developed model is characterized by diffuse alveolar damage to the lungs and high mortality rates, as well as by a multifold increase in the mRNA level of interleukin-6 in the lungs. The model can be used for assessing the efficacy of drug candidates in the treatment of acute lung injury and ARDS, including in COVID-19.


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