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Text
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URL Address
<a href="http://doi.org/10.1152/ajplung.90629.2008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.90629.2008</a>
Pages
L487–495
Issue
3
Volume
297
Dublin Core
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Title
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Beta-adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure.
Publisher
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American journal of physiology. Lung cellular and molecular physiology
Date
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2009
2009-09
Subject
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Adrenergic; Animals; beta/*metabolism; Body Fluids/*metabolism; Epithelial Cells/drug effects/metabolism/pathology; Gene Expression Regulation/drug effects; Heart Failure/blood/diagnostic imaging/*metabolism/*pathology; Hormones/blood; Hyperplasia; Ion Channels/genetics/metabolism; Male; Messenger/genetics/metabolism; Myocardial Infarction/blood/diagnostic imaging/pathology; Pulmonary Alveoli/drug effects/*pathology; Rats; Receptors; RNA; Sprague-Dawley; Terbutaline/pharmacology; Ultrasonography
Creator
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Maron Michael B; Luther Daniel J; Pilati Charles F; Ohanyan Vahagn; Li Tianbo; Koshy Shyny; Horne Walter I; Meszaros J Gary; Walro Jon M; Folkesson Hans G
Description
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The alveolar epithelium plays a critical role in resolving pulmonary edema. We thus hypothesized that its function might be upregulated in rats with heart failure, a condition that severely challenges the lung's ability to maintain fluid balance. Heart failure was induced by left coronary artery ligation. Echocardiographic and cardiovascular hemodynamics confirmed its development at 16 wk postligation. At that time, alveolar fluid clearance was measured by an increase in protein concentration over 1 h of a 5% albumin solution instilled into the lungs. Baseline alveolar fluid clearance was similar in heart failure and age-matched control rats. Terbutaline was added to the instillate to determine whether heart failure rats responded to beta-adrenoceptor stimulation. Alveolar fluid clearance in heart failure rats was increased by 194% after terbutaline stimulation compared with a 153% increase by terbutaline in control rats. To determine the mechanisms responsible for this accelerated alveolar fluid clearance, we measured ion transporter expression (ENaC, Na-K- ATPase, CFTR). No significant upregulation was observed for these ion transporters in the heart failure rats. Lung morphology showed significant alveolar epithelial type II cell hyperplasia in heart failure rats. Thus, alveolar epithelial type II cell hyperplasia is the likely explanation for the increased terbutaline-stimulated alveolar fluid clearance in heart failure rats. These data provide evidence for previously unrecognized mechanisms that can protect against or hasten resolution of alveolar edema in heart failure.
Identifier
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<a href="http://doi.org/10.1152/ajplung.90629.2008" target="_blank" rel="noreferrer noopener">10.1152/ajplung.90629.2008</a>
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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).
2009
Adrenergic
American journal of physiology. Lung cellular and molecular physiology
Animals
beta/*metabolism
Body Fluids/*metabolism
Department of Integrative Medical Sciences
Epithelial Cells/drug effects/metabolism/pathology
Folkesson Hans G
Gene Expression Regulation/drug effects
Heart Failure/blood/diagnostic imaging/*metabolism/*pathology
Hormones/blood
Horne Walter I
Hyperplasia
Ion Channels/genetics/metabolism
Koshy Shyny
Li Tianbo
Luther Daniel J
Male
Maron Michael B
Messenger/genetics/metabolism
Meszaros J Gary
Myocardial Infarction/blood/diagnostic imaging/pathology
NEOMED College of Medicine
Ohanyan Vahagn
Pilati Charles F
Pulmonary Alveoli/drug effects/*pathology
Rats
Receptors
RNA
Sprague-Dawley
Terbutaline/pharmacology
Ultrasonography
Walro Jon M