ArticleAmerican journal of respiratory cell and molecular biology2014
Antifibrinolytic mechanisms in acute airway injury after sulfur mustard analog inhalation.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Cannabinoid-2 Receptor Activation Attenuates Sulfur Mustard Analog 2-Chloroethyl-Ethyl-Sulfide-Induced Acute Lung Injury in Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Overlapping Science in Radiation and Sulfur Mustard Exposures of Skin and Lung: Consideration of Models, Mechanisms, Organ Systems, and Medical Countermeasures: Overlapping science in radiation and sulfur mustard injuries to lung and skin.Disaster medicine and public health preparedness · 2023Article
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Alleviation of methyl isocyanate-induced airway obstruction and mortality by tissue plasminogen activator.Annals of the New York Academy of Sciences · 2020Article
- MicroRNA-mediated inflammation and coagulation effects in rats exposed to an inhaled analog of sulfur mustard.Annals of the New York Academy of Sciences · 2020Article
- Acute cytotoxicity and increased vascular endothelial growth factor after in vitro nitrogen mustard vapor exposure.Annals of the New York Academy of Sciences · 2020Article
- Extracellular nucleic acid scavenging rescues rats from sulfur mustard analog-induced lung injury and mortality.Archives of toxicology · 2020Article
- Fibrinolysis Shutdown in Trauma: Historical Review and Clinical Implications.Anesthesia and analgesia · 2019Review
- Methyl isocyanate inhalation induces tissue factor-dependent activation of coagulation in rats.Drug and chemical toxicology · 2019Article
- Bronchiolitis Obliterans and Pulmonary Fibrosis after Sulfur Mustard Inhalation in Rats.American journal of respiratory cell and molecular biology · 2018Article
- Editor's Highlight: Pulmonary Vascular Thrombosis in Rats Exposed to Inhaled Sulfur Mustard.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- From the Cover: ImpairedProliferation and Differentiation of the Conducting Airway Epithelium Associated With Bronchiolitis Obliterans After Sulfur Mustard Inhalation Injury in Rats.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- An Official American Thoracic Society Workshop Report: Chemical Inhalational Disasters. Biology of Lung Injury, Development of Novel Therapeutics, and Medical Preparedness.Annals of the American Thoracic Society · 2017Article
- Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 2016Review
- Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy.Annals of the New York Academy of Sciences · 2016Review
- Emerging targets for treating sulfur mustard-induced injuries.Annals of the New York Academy of Sciences · 2016Review
- Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals.Biochemical pharmacology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury in response to mustard gas (sulfur mustard [SM]) inhalation results in formation of fibrin casts, which obstruct the airway. The objective of this study was to identify fibrinolytic pathways that could be contributing to the persistence of airway casts after SM exposure. Rats were exposed to the SM analog, 2-chloroethyl ethyl sulfide, via nose-only aerosol inhalation. At 4 and 18 hours after exposure, animals were killed and airway-capillary leak estimated by measuring bronchoalveolar lavage fluid (BALF) protein and IgM content. The fibrin clot-degrading and plasminogen-activating capabilities of BALF were also assessed by activity assays, whereas Western blotting was used to determine the presence and activities of plasminogen activator inhibitor-1, thrombin activatable fibrinolytic inhibitor and α2-antiplasmin. Measurement of tissue-specific steady-state mRNA levels was also conducted for each fibrinolytic inhibitor to assess whether its synthesis occurs in lung or at extrapulmonary sites. The results of this study demonstrate that fibrin-degrading and plasminogen-activating capabilities of the airways become impaired during the onset of 2-chloroethyl ethyl sulfide-induced vascular leak. Findings of functionally active reservoirs of plasminogen activator inhibitor-1, thrombin activatable fibrinolysis inhibitor, and α2-antiplasmin in BALF indicate that airway fibrinolysis is inhibited at multiple levels in response to SM.
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