Document Detail


Hypercapnia: a nonpermissive environment for the lung.
MedLine Citation:
PMID:  22246860     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
István Vadász; Rolf D Hubmayr; Nicolás Nin; Peter H S Sporn; Jacob I Sznajder
Publication Detail:
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:
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:
Created Date:  2012-04-04     Completed Date:  2012-06-11     Revised Date:  2014-10-16    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  417-21     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acute Lung Injury / 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:
HL-41829/HL/NHLBI NIH HHS; HL-85534/HL/NHLBI NIH HHS; R01 HL085534/HL/NHLBI NIH HHS; R37 HL048129/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
142M471B3J/Carbon Dioxide
Comments/Corrections

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