| Hypercapnia: a nonpermissive environment for the lung. | |
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MedLine Citation:
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PMID: 22246860 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Patients with severe acute and chronic lung diseases develop derangements in gas exchange that may result in increased levels of CO(2) (hypercapnia), the effects of which on human health are incompletely understood. It has been proposed that hypercapnia may have beneficial effects in patients with acute lung injury, and the concepts of "permissive" and even "therapeutic" hypercapnia have emerged. However, recent work suggests that CO(2) can act as a signaling molecule via pH-independent mechanisms, resulting in deleterious effects in the lung. Here we review recent research on how elevated CO(2) is sensed by cells in the lung and the potential harmful effects of hypercapnia on epithelial and endothelial barrier, lung edema clearance, innate immunity, and host defense. In view of these findings, we raise concerns about the potentially deleterious effects hypercapnia may have in patients with acute and chronic lung diseases. |
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Authors:
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István Vadász; Rolf D Hubmayr; Nicolás Nin; Peter H S Sporn; Jacob I Sznajder |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review Date: 2012-01-12 |
Journal Detail:
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Title: American journal of respiratory cell and molecular biology Volume: 46 ISSN: 1535-4989 ISO Abbreviation: Am. J. Respir. Cell Mol. Biol. Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-04-04 Completed Date: 2012-06-11 Revised Date: 2013-04-01 |
Medline Journal Info:
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Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 417-21 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Giessen Lung Center, Justus Liebig University, Germany. istvan.vadasz@innere.med.uni-giessen.de |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Lung Injury
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metabolism* Carbon Dioxide / blood* Cell Membrane / metabolism Humans Hypercapnia / etiology* Immunity, Innate Lung Pulmonary Alveoli / cytology, metabolism Pulmonary Edema / etiology Respiration, Artificial |
| Grant Support | |
ID/Acronym/Agency:
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HL-41829/HL/NHLBI NIH HHS; HL-85534/HL/NHLBI NIH HHS; R01 HL085534/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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124-38-9/Carbon Dioxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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