Document Detail


The action of beta-receptors on microvascular endothelium or: is airways plasma exudation inhibited by beta-agonists?
MedLine Citation:
PMID:  8099694     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The connections between airway inflammation, plasma exudation and a possible anti-exudative action of beta-agonists are discussed. Asthma involves a response to inflammatory mediators which results in increased microvascular leakage with exudation of plasma into the airways. This plasma exudation is a specific inflammatory response and also a general response in the sense that it is independent of the mechanism sustaining the inflammation. Thus, mucosal exudation of plasma may reflect the subepithelial airway inflammatory process, irrespective of its genesis. In addition, the exudate itself contains many substances which may themselves promote inflammation and be major factors in producing and sustaining acute and chronic airway inflammation. This suggests that drug therapies should be aimed at reducing plasma exudation. Studies in guinea pigs have shown that a number of drugs such as xanthines, cromoglycates, glucocorticoids and beta-agonists may inhibit this exudation, but the effect seems to be attenuated in human mucosal tissue. beta-Agonists appear promising in this respect, but if an anti-exudative effect is confirmed for them, it will be necessary to determine whether this is a direct effect or secondary to their effects on cellular inflammatory processes in the airways.
Authors:
C G Persson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Life sciences     Volume:  52     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  1993  
Date Detail:
Created Date:  1993-07-13     Completed Date:  1993-07-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2111-21     Citation Subset:  IM    
Affiliation:
Department of Clinical Pharmacology, University Hospital, Lund, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology*
Animals
Asthma / drug therapy*,  physiopathology
Bronchial Hyperreactivity / drug therapy
Capillary Permeability / drug effects
Endothelium, Vascular / drug effects*
Exudates and Transudates / drug effects*
Humans
Respiratory System / blood supply,  drug effects*
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists

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


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