| Physiologic dysfunction of the asthmatic lung: what's going on down there, anyway? | |
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MedLine Citation:
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PMID: 19387035 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Asthma is a syndrome of lung dysfunction characterized by airflow obstruction, reversibility to bronchodilators, and airways hyperresponsiveness (AHR). There is a growing body of evidence that suggests that the principle defect in asthma is the occlusion of the airway lumen by liquid, fibrin, and mucus. The fall in FEV(1) observed in asthma is best explained by a loss of communicating airspaces and the rise in residual lung volume. Imaging studies in both human patients and experimental animals support this hypothesis. An increased propensity for the airways to close can be a cause of AHR. We conclude that loss of lung volume plays a central role in determining the dysfunction of the asthmatic lung as measured by FEV(1). Together, these recent findings provide a better understanding of the causes of airflow obstruction and AHR, suggesting new avenues for the development of more effective asthma therapies. |
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Authors:
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Charles G Irvin; Jason H T Bates |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Proceedings of the American Thoracic Society Volume: 6 ISSN: 1546-3222 ISO Abbreviation: Proc Am Thorac Soc Publication Date: 2009 May |
Date Detail:
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Created Date: 2009-04-23 Completed Date: 2009-07-10 Revised Date: 2010-09-27 |
Medline Journal Info:
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Nlm Unique ID: 101203596 Medline TA: Proc Am Thorac Soc Country: United States |
Other Details:
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Languages: eng Pagination: 306-11 Citation Subset: IM |
Affiliation:
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Department of Medicine, Vermont Lung Center, University of Vermont, Burlington, VT 05405-0075, USA. charles.irvin@uvm.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Asthma / pathology, physiopathology* Bronchial Hyperreactivity / pathology, physiopathology Humans Models, Animal Respiratory Mechanics Severity of Illness Index |
| Grant Support | |
ID/Acronym/Agency:
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5 P20 RR15557/RR/NCRR NIH HHS; HL 67273/HL/NHLBI NIH HHS; R01 HL075593/HL/NHLBI NIH HHS; R01 HL080258/HL/NHLBI NIH HHS |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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