Spectroscopic Approach to Capillary‐Alveolar Membrane Damage Induced Acute Lung Injury

Wang, Jing; Oppenheimer, L.; Fata, Paola; Pintin, Julio; Stimpson, Ross; Mantsch, Henry H.

doi:10.1155/1999/678708

Cited by 6 publications

(3 citation statements)

References 16 publications

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“…In this patient, assist-control ventilation and weaning were difficult since two components were present: increased airway resistance and decreased lung compliance. However, at variance with most reported studies of a poor prognosis of increased permeability pulmonary oedema, with some 50±60% of patients dying [17], the prognosis here was good without important sequelae. This could be due to the fact that, in this patient, the underlying cause was self-limiting, i.e.…”

Section: Discussioncontrasting

confidence: 95%

Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents

Mapp

Pozzato

Pavoni³

et al. 2000

Eur Respir J

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Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents. C.E. Mapp, V. Pozzato, V. Pavoni, G. Gritti #ERS Journals Ltd 2000. ABSTRACT: This report presents a case of severe asthmatic attack and adult respiratory distress syndrome, which occurred in an asthmatic subject following acute short-term exposure to commonly used cleaning detergents. Premorbid lung conditions, i.e. asthma and airway hyperresponsiveness, might have been risk factors for illness severity but not for persistent complaints.This case report indicates that nonindustrial exposures due to household product misuse, especially to mixing cleaning agents, may cause adult respiratory distress syndrome and not only irritant-induced asthma. Eur Respir J 2000; 16: 570±572. This study was supported by Ministero dell' Universita' e della Ricerca Scientifica e Technologica (60% and 40%) and Associazione per la Ricerca e la Curadell' Asma.

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Section: Discussioncontrasting

confidence: 95%

Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents

Mapp

Pozzato

Pavoni³

et al. 2000

Eur Respir J

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“…At present, Bax, Bcl-2 and caspase-3 have been established to be associated with ARDS (38). ARDS is caused by alveolar-capillary membrane injury triggering pulmonary edema and atelectasis (39). During this process, progressive apoptosis occurs in the alveolar epithelium and pulmonary vascular endothelial cells (40).…”

Section: Discussionmentioning

confidence: 99%

Penehyclidine hydrochloride alleviates lipopolysaccharide‑induced acute respiratory distress syndrome in cells via regulating autophagy‑related pathway

Wang

Liu

et al. 2020

Mol Med Rep

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Acute progressive hypoxic respiratory failure caused by various predisposing factors is known as acute respiratory distress syndrome (ARDS). Although penehyclidine hydrochloride (PHC), an anticholinergic drug, is widely applied in clinical practice, the specific mechanisms underlying PHC in the treatment of ARDS are not completely understood. In the present study, BEAS-2B cells were treated with 10 ng/ml lipopolysaccharide (LPS) to establish an ARDS cell model and a rat model of acute lung injury (ALI). The influences of PHC and/or autophagy inhibitor (3-methyladenine (3-MA)) on the morphology, autophagy, proliferation and apoptosis of cells and tissues were evaluated using hematoxylin and eosin staining, Cell Counting Kit-8 assays, Hoechst staining, TUNEL staining, flow cytometry, immunofluorescence assays, ELISAs and scanning electron microscopy. The expression levels of apoptosis-and autophagy-related proteins were measured via western blotting. The results indicated that PHC enhanced proliferation and autophagy, and decreased apoptosis and the inflammatory response in LPS-induced BEAS-2B cells and ALI model rats. In addition, 3-MA reversed the effects of PHC on proliferation, inflammation, apoptosis and autophagy in LPS-induced BEAS-2B cells. Therefore, the present study suggested that PHC demonstrated a protective effect in LPS-induced ARDS by regulating an autophagy-related pathway.

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“…Experimental evidence has shown that the alveolar-capillary leak allows bidirectional travel of fluid and proteins. In contrast to normal lungs, the lungs of ARDS patients who are administered with an intravenous injection of hetastarch have an accumulation of this molecule in the airspaces (Wang et al, 1999). In addition, patients with ARDS have elevated plasma levels of surfactant proteins that are only produced by lung alveolar epithelial cells (Doyle et al, 1997).…”

Section: Clinical Puzzlementioning

confidence: 99%

Development of animal models for the acute respiratory distress syndrome

Bastarache

Blackwell

2009

Disease Models &Amp; Mechanisms

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Injury to the lung parenchyma results in the acute respiratory distress syndrome (ARDS), which is a common and life-threatening cause of respiratory failure and mortality that develops after a variety of insults, including sepsis, multiple trauma, pneumonia, aspiration of gastric contents and severe burns. The pathogenesis of ARDS is complex with loss of the alveolar-capillary barrier and flooding of the airspaces with protein-rich fluid; injury to the alveolar epithelium; an influx of neutrophils and macrophages; and fibrin deposition as a result of activation of coagulation and inhibition of fibrinolysis. These changes develop over hours to a few days after the initiating event and often take days or weeks to resolve. Despite decades of research, there is only one therapy (low tidal volume ventilation) that has been shown to reduce mortality in ARDS. Further research into the pathogenesis of this devastating condition is crucial for the development of novel and specific therapies that target specific disease mechanisms. Unfortunately, no single animal model of ARDS replicates the complex pathophysiological changes seen in patients. This is a severe limitation in the study of ARDS and has impaired scientific and therapeutic progress in this field. Here, we discuss the primary features of this syndrome, highlight limitations of current animal models and suggest new approaches to investigate key components of pathogenesis. Hopefully, as new technologies and approaches emerge, barriers to scientific progress in ARDS will be overcome.

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Spectroscopic Approach to Capillary‐Alveolar Membrane Damage Induced Acute Lung Injury

Cited by 6 publications

References 16 publications

Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents

Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents

Penehyclidine hydrochloride alleviates lipopolysaccharide‑induced acute respiratory distress syndrome in cells via regulating autophagy‑related pathway

Development of animal models for the acute respiratory distress syndrome

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