ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Postexposure aerosolized heparin reduces lung injury in chlorine-exposed mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Phosgene inhalation injury in mice: Modeling human pathophysiology, biomarker discovery, and therapeutic target identification.Toxicology and applied pharmacology · 2026Article
- The long road to Ithaca: a physiologist's journey.American journal of physiology. Cell physiology · 2025Review
- Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024Review
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Toxic effects of chlorine gas and potential treatments: a literature review.Toxicology mechanisms and methods · 2021Review
- Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.Annals of the New York Academy of Sciences · 2020Article
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Disease-modifying treatment of chemical threat agent-induced acute lung injury.Annals of the New York Academy of Sciences · 2020Review
- Nebulised heparin as a treatment for COVID-19: scientific rationale and a call for randomised evidence.Critical care (London, England) · 2020Review
- Phosgene inhalation causes hemolysis and acute lung injury.Toxicology letters · 2019Article
- Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome.Chinese medical journal · 2018Review
- Nebulized anticoagulants in lung injury in critically ill patients-an updated systematic review of preclinical and clinical studies.Annals of translational medicine · 2017Review
- 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
- Heme Attenuation Ameliorates Irritant Gas Inhalation-Induced Acute Lung Injury.Antioxidants & redox signaling · 2016Article
- Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Chlorine inhalation-induced myocardial depression and failure.Physiological reports · 2015Article
- A critical review of the American Journal of Physiology-Lung Cellular and Molecular Physiology: 2012-2015.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Inhaled matters of the heart.Cardiovascular regenerative medicineArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlorine (Cl2) is a highly reactive oxidant gas that, when inhaled, may cause acute lung injury culminating in death from respiratory failure. In this study, we tested the hypothesis that exposure of mice to Cl2 causes intra-alveolar and systemic activation of the coagulation cascade that plays an important role in development of lung injury. C57Bl/6 mice were exposed to Cl2 (400 for 30 min or 600 ppm for 45 min) in environmental chambers and then returned to room air for 1 or 6 h. Native coagulation (NATEM) parameters such as blood clotting time and clot formation time were measured in whole blood by the viscoelastic technique. D-dimers and thrombin-anti-thrombin complexes were measured in both plasma and bronchoalveolar lavage fluid (BALF) by ELISA. Our results indicate that mice exposed to Cl2 gas had significantly increased clotting time, clot formation time, and D-dimers compared with controls. The thrombin-anti-thrombin complexes were also increased in the BALF of Cl2 exposed animals. To test whether increased coagulation contributed to the development of acute lung injury, mice exposed to Cl2 and returned to room air were treated with aerosolized heparin or vehicle for 20 min. Aerosolized heparin significantly reduced protein levels and the number of inflammatory cells in the BALF at 6 h postexposure. These findings highlight the importance of coagulation abnormities in the development of Cl2-induced lung injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.