Nebulized prostaycclin (PGI2) in acute respiratory distress syndrome: Impact of primary (pulmonary injury) and secondary (extrapulmonary injury) disease on gas exchange response

2001 ◽  
Vol 29 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Guido Domenighetti ◽  
Hans Stricker ◽  
Brigitte Waldispuehl
2020 ◽  
Vol 125 (5) ◽  
pp. e437-e438
Author(s):  
Silvia Coppola ◽  
Tommaso Pozzi ◽  
Mattia Busana ◽  
Francesca Bichi ◽  
Virginia Camponetti ◽  
...  

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Vincent Bonny ◽  
Vincent Janiak ◽  
Savino Spadaro ◽  
Andrea Pinna ◽  
Alexandre Demoule ◽  
...  

An amendment to this paper has been published and can be accessed via the original article.


2005 ◽  
Vol 20 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Eric A. J. Hoste ◽  
Carl D. V. K. Roosens ◽  
Steven Bracke ◽  
Johan M. A. Decruyenaere ◽  
Dominique D. Benoit ◽  
...  

2020 ◽  
Author(s):  
Xianyu Mu ◽  
Hongrong Wang ◽  
Haiyong Li

Abstract Background: This study aimed to explore the function of long noncoding RNA H19 (H19) on pulmonary injury, inflammation and fibrosis in lipoproteins (LPS)-induced acute respiratory distress syndrome (ARDS) rats. Methods: The LPS-induced ARDS rat model was established by intratracheal instillation with 2 mg/kg LPS. QRT-PCR was performed to detect the expression of H19, miR-423-5p, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6,, monocyte chemoattractant protein (MCP)-1 and vascular endothelial growth factor (VEGF). Histology score was detected by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines and the concentration of VEGF in bronchoalveolar lavage fluid (BALF). The protein expression of fiber factors was measured by western blot. The degree of fibrosis was observed by masson-trichrome staining. Dual-luciferase reporter assay was used to determine the binding site between miR-423-5p and H19.Results: The expression of H19 was significantly increased, while miR-423-5p was decreased in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1 and VEGF in LPS-induced ARDS rats, and decreased the levels of TNF-α, IL-1β, IL-6and the concentration of VEGF in BALF, histology score of LPS-induced ARDS rats. H19 inhibition also decreased the fibrosis score and the proteins expression of fiber factors of LPS-induced ARDS rats. Furthermore, miR-423-5p eliminated the effect of H19 on LPS-induced MH-S cells.Conclusions: Silencing of H19 ameliorated the pulmonary injury, inflammation and fibrosis of LPS-induced ARDS through regulating miR-423-5p, which may be a promising therapeutic strategy to treat ARDS.


2020 ◽  
Vol 2 (1) ◽  
pp. 74-80
Author(s):  
Anisa Ramadhanti

Rokok elektronik atau vape diklaim lebih aman dan lebih tidak berbahaya karena lebih sedikit mengandung bahan kimia toksik dibandingkan rokok konvensional. Walaupun demikian, masih banyak pihak yang mempertanyakan keamanan rokok elektronik. Liquid dalam rokok elektronik dan aerosol yang dihasilkan terbukti mengandung sejumlah komponen kimia yang kemungkinan memiliki efek yang berbahaya terhadap kesehatan, terutama paru yang dapat menyebabkan vaping-associated pulmonary injury (VAPI). Berdasarkan laporan kasus sebelumnya, VAPI terbagi menjadi beberapa spektrum penyakit, diantaranya adalah pneumonia eosinofilik akut, organizing pneumonia, lipoid pneumonia, kerusakan alveolus difus, dan acute respiratory distress syndrome (ARDS), perdarahan alveolar difus, pneumonitis hipersensitif, dan yang paling jarang yaitu giant-cell interstitial pneumonitis. Terdapat definisi kasus yang terbaru dalam menegakkan diagnosis VAPI, serta tatalaksana


2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Yufeng Liang ◽  
Junjie Xie ◽  
Di Che ◽  
Chunmin Zhang ◽  
Yongmin Lin ◽  
...  

Abstract Background: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury that has a high mortality rate and leads to substantial healthcare costs. MicroRNA-124-3p (miR-124-3p) helps to suppress inflammation during a pulmonary injury. However, its mechanism of action is largely unknown, and its role in ARDS remains to be determined. Methods: Mice and NR8383 cells were exposed to lipopolysaccharides (LPS) to induce ARDS, and their miR-124-3p levels were determined. After a miRNA agomir was administrated to the mice, their pulmonary injuries were evaluated by H&E staining and assays for peripheral inflammatory cytokine levels. The direct interaction between miR-124-3p and p65 was predicted, and then confirmed by a luciferase activity assay. The role played by miRNA-124-3p in regulating p65 expression was further examined by transfection with its agomir, and its role in cell apoptosis was investigated by observing the effects of miRNA overexpression in vitro and in vivo. Results: After exposure to LPS, there was a consistent decrease in miR-124-3p expression in the lungs of mice and in NR8383 cells. After treatment with the miR-124-3p agomir, the degrees of pulmonary injury (e.g. alveolar hemorrhage and interstitial edema), and the increases in IL-1β, IL-6, and TNF-α levels induced by LPS were significantly attenuated. Overexpression of miR-124-3p in NC8383 cells and lung tissues significantly suppressed LPS-induced p65 expression and cell apoptosis. Conclusions: These results suggest that miR-124-3p directly targeted p65, and thereby decreased the levels of inflammation and pulmonary injury in a mouse model of ARDS.


2021 ◽  
Vol 12 ◽  
Author(s):  
Fernando Suárez-Sipmann ◽  
Jesús Villar ◽  
Carlos Ferrando ◽  
Juan A. Sánchez-Giralt ◽  
Gerardo Tusman

Mechanical ventilation (MV) is a lifesaving supportive intervention in the management of acute respiratory distress syndrome (ARDS), buying time while the primary precipitating cause is being corrected. However, MV can contribute to a worsening of the primary lung injury, known as ventilation-induced lung injury (VILI), which could have an important impact on outcome. The ARDS lung is characterized by diffuse and heterogeneous lung damage and is particularly prone to suffer the consequences of an excessive mechanical stress imposed by higher airway pressures and volumes during MV. Of major concern is cyclic overdistension, affecting those lung segments receiving a proportionally higher tidal volume in an overall reduced lung volume. Theoretically, healthier lung regions are submitted to a larger stress and cyclic deformation and thus at high risk for developing VILI. Clinicians have difficulties in detecting VILI, particularly cyclic overdistension at the bedside, since routine monitoring of gas exchange and lung mechanics are relatively insensitive to this mechanism of VILI. Expired CO2 kinetics integrates relevant pathophysiological information of high interest for monitoring. CO2 is produced by cell metabolism in large daily quantities. After diffusing to tissue capillaries, CO2 is transported first by the venous and then by pulmonary circulation to the lung. Thereafter diffusing from capillaries to lung alveoli, it is finally convectively transported by lung ventilation for its elimination to the atmosphere. Modern readily clinically available sensor technology integrates information related to pulmonary ventilation, perfusion, and gas exchange from the single analysis of expired CO2 kinetics measured at the airway opening. Current volumetric capnography (VCap), the representation of the volume of expired CO2 in one single breath, informs about pulmonary perfusion, end-expiratory lung volume, dead space, and pulmonary ventilation inhomogeneities, all intimately related to cyclic overdistension during MV. Additionally, the recently described capnodynamic method provides the possibility to continuously measure the end-expiratory lung volume and effective pulmonary blood flow. All this information is accessed non-invasively and breath-by-breath helping clinicians to personalize ventilatory settings at the bedside and minimize overdistension and cyclic deformation of lung tissue.


Sign in / Sign up

Export Citation Format

Share Document