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Text
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URL Address
<a href="http://doi.org/10.1152/ajplung.00395.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00395.2011</a>
Pages
L259–271
Issue
3
Volume
303
Dublin Core
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Title
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The adenosine 2A receptor agonist GW328267C improves lung function after acute lung injury in rats.
Publisher
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American journal of physiology. Lung cellular and molecular physiology
Date
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2012
2012-08
Subject
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Acute Lung Injury/*drug therapy/metabolism/pathology; Adenosine A2A/*chemistry; Adenosine/*analogs & derivatives/therapeutic use; Amiloride/pharmacology; Animals; Biological Transport; Bronchoalveolar Lavage; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism; Endotoxemia/*drug therapy/metabolism/microbiology; Epithelial Sodium Channel Blockers; Epithelial Sodium Channels/metabolism; Escherichia coli; Escherichia coli Infections/drug therapy/metabolism/microbiology; Immunoblotting; Male; Pneumonia/*drug therapy/metabolism/microbiology; Pulmonary Alveoli/cytology/*drug effects/metabolism; Pulmonary Edema/*drug therapy/metabolism/pathology; Rats; Receptor; Respiratory Physiological Phenomena; Sodium Channel Blockers/pharmacology; Sprague-Dawley; Triazoles/*therapeutic use
Creator
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Folkesson Hans G; Kuzenko Stephanie R; Lipson David A; Matthay Michael A; Simmons Mark A
Description
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There is a significant unmet need for treatments of patients with acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). The primary mechanism that leads to resolution of alveolar and pulmonary edema is active vectorial Na(+) and Cl(-) transport across the alveolar epithelium. Several studies have suggested a role for adenosine receptors in regulating this fluid transport in the lung. Furthermore, these studies point to the A(2A) subtype of adenosine receptor (A(2A)R) as playing a role to enhance fluid transport, suggesting that activation of the A(2A)R may enhance alveolar fluid clearance (AFC). The current studies test the potential therapeutic value of the A(2A)R agonist GW328267C to accelerate resolution of alveolar edema and ALI/ARDS in rats. GW328267C, at concentrations of 10(-5) M to 10(-3) M, instilled into the airspaces, increased AFC in control animals. GW328267C did not increase AFC beyond that produced by maximal beta-adrenergic stimulation. The effect of GW328267C was inhibited by amiloride but was not affected by cystic fibrosis transmembrane conductance regulator inhibition. The drug was tested in three models of ALI, HCl instillation 1 h, LPS instillation 16 h, and live Escherichia coli instillation 2 h before GW328267C instillation. After either type of injury, GW328267C (10(-4) M) decreased pulmonary edema formation and restored AFC, measured 1 h after GW328267C instillation. These findings show that GW328267C has beneficial effects in experimental models of ALI and may be a useful agent for treating patients with ALI or prophylactically to prevent ALI.
Identifier
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<a href="http://doi.org/10.1152/ajplung.00395.2011" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00395.2011</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Acute Lung Injury/*drug therapy/metabolism/pathology
Adenosine A2A/*chemistry
Adenosine/*analogs & derivatives/therapeutic use
American journal of physiology. Lung cellular and molecular physiology
Amiloride/pharmacology
Animals
Biological Transport
Bronchoalveolar Lavage
Cystic Fibrosis Transmembrane Conductance Regulator/metabolism
Endotoxemia/*drug therapy/metabolism/microbiology
Epithelial Sodium Channel Blockers
Epithelial Sodium Channels/metabolism
Escherichia coli
Escherichia coli Infections/drug therapy/metabolism/microbiology
Folkesson Hans G
Immunoblotting
Kuzenko Stephanie R
Lipson David A
Male
Matthay Michael A
Pneumonia/*drug therapy/metabolism/microbiology
Pulmonary Alveoli/cytology/*drug effects/metabolism
Pulmonary Edema/*drug therapy/metabolism/pathology
Rats
Receptor
Respiratory Physiological Phenomena
Simmons Mark A
Sodium Channel Blockers/pharmacology
Sprague-Dawley
Triazoles/*therapeutic use