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β(2 )adrenergic agonists in acute lung injury? The heart of the matter

Despite extensive research into its pathophysiology, acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating syndrome with mortality approaching 40%. Pharmacologic therapies that reduce the severity of lung injury in vivo and in vitro have not yet been translated to ef...

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Detalles Bibliográficos
Autor principal: Lee, Jae W
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811950/
https://www.ncbi.nlm.nih.gov/pubmed/20017898
http://dx.doi.org/10.1186/cc8171
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author Lee, Jae W
author_facet Lee, Jae W
author_sort Lee, Jae W
collection PubMed
description Despite extensive research into its pathophysiology, acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating syndrome with mortality approaching 40%. Pharmacologic therapies that reduce the severity of lung injury in vivo and in vitro have not yet been translated to effective clinical treatment options, and innovative therapies are needed. Recently, the use of β(2 )adrenergic agonists as potential therapy has gained considerable interest due to their ability to increase the resolution of pulmonary edema. However, the results of clinical trials of β agonist therapy for ALI/ARDS have been conflicting in terms of benefit. In the previous issue of Critical Care, Briot and colleagues present evidence that may help clarify the inconsistent results. The authors demonstrate that, in oleic acid lung injury in dogs, the inotropic effect of β agonists may recruit damaged pulmonary capillaries, leading to increased lung endothelial permeability.
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spelling pubmed-28119502010-12-07 β(2 )adrenergic agonists in acute lung injury? The heart of the matter Lee, Jae W Crit Care Commentary Despite extensive research into its pathophysiology, acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating syndrome with mortality approaching 40%. Pharmacologic therapies that reduce the severity of lung injury in vivo and in vitro have not yet been translated to effective clinical treatment options, and innovative therapies are needed. Recently, the use of β(2 )adrenergic agonists as potential therapy has gained considerable interest due to their ability to increase the resolution of pulmonary edema. However, the results of clinical trials of β agonist therapy for ALI/ARDS have been conflicting in terms of benefit. In the previous issue of Critical Care, Briot and colleagues present evidence that may help clarify the inconsistent results. The authors demonstrate that, in oleic acid lung injury in dogs, the inotropic effect of β agonists may recruit damaged pulmonary capillaries, leading to increased lung endothelial permeability. BioMed Central 2009 2009-12-07 /pmc/articles/PMC2811950/ /pubmed/20017898 http://dx.doi.org/10.1186/cc8171 Text en Copyright ©2009 BioMed Central Ltd
spellingShingle Commentary
Lee, Jae W
β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title_full β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title_fullStr β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title_full_unstemmed β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title_short β(2 )adrenergic agonists in acute lung injury? The heart of the matter
title_sort β(2 )adrenergic agonists in acute lung injury? the heart of the matter
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811950/
https://www.ncbi.nlm.nih.gov/pubmed/20017898
http://dx.doi.org/10.1186/cc8171
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