Document Detail

Hypercapnia induces injury to alveolar epithelial cells via a nitric oxide-dependent pathway.
MedLine Citation:
PMID:  11053037     Owner:  NLM     Status:  MEDLINE    
Ventilator strategies allowing for increases in carbon dioxide (CO(2)) tensions (hypercapnia) are being emphasized to ameliorate the consequences of inflammatory-mediated lung injury. Inflammatory responses lead to the generation of reactive species including superoxide (O(2)(-)), nitric oxide (.NO), and their product peroxynitrite (ONOO(-)). The reaction of CO(2) and ONOO(-) can yield the nitrosoperoxocarbonate adduct ONOOCO(2)(-), a more potent nitrating species than ONOO(-). Based on these premises, monolayers of fetal rat alveolar epithelial cells were utilized to investigate whether hypercapnia would modify pathways of.NO production and reactivity that impact pulmonary metabolism and function. Stimulated cells exposed to 15% CO(2) (hypercapnia) revealed a significant increase in.NO production and nitric oxide synthase (NOS) activity. Cell 3-nitrotyrosine content as measured by both HPLC and immunofluorescence staining also increased when exposed to these same conditions. Hypercapnia significantly enhanced cell injury as evidenced by impairment of monolayer barrier function and increased induction of apoptosis. These results were attenuated by the NOS inhibitor N-monomethyl-L-arginine. Our studies reveal that hypercapnia modifies.NO-dependent pathways to amplify cell injury. These results affirm the underlying role of.NO in tissue inflammatory reactions and reveal the impact of hypercapnia on inflammatory reactions and its potential detrimental influences.
J D Lang; P Chumley; J P Eiserich; A Estevez; T Bamberg; A Adhami; J Crow; B A Freeman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  279     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2000 Nov 
Date Detail:
Created Date:  2000-11-01     Completed Date:  2000-11-09     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L994-1002     Citation Subset:  IM    
Department of Anesthesiology, The University of Alabama at Birmingham, Birmingham, Alabama 35233-4234, USA.
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MeSH Terms
Apoptosis / drug effects,  physiology*
Carbon Dioxide / pharmacology*
Cells, Cultured
Cytokines / pharmacology*
Interferon-gamma / pharmacology
Interleukin-1 / pharmacology
Lipopolysaccharides / pharmacology
Nitrates / metabolism
Nitric Oxide / physiology*
Nitric Oxide Synthase / metabolism
Pulmonary Alveoli / cytology*
Respiratory Mucosa / cytology*,  drug effects,  physiology*
Tumor Necrosis Factor-alpha / pharmacology
Tyrosine / analogs & derivatives*,  analysis
omega-N-Methylarginine / pharmacology
Grant Support
Reg. No./Substance:
0/Cytokines; 0/Interleukin-1; 0/Lipopolysaccharides; 0/Nitrates; 0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide; 124-38-9/Carbon Dioxide; 17035-90-4/omega-N-Methylarginine; 26404-66-0/peroxynitric acid; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; 82115-62-6/Interferon-gamma; EC Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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