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Resolution of Pulmonary Edema: Thirty Years of Progress

American journal of respiratory and critical care medicine, 2014-06, Vol.189 (11), p.1301-1308 [Peer Reviewed Journal]

2015 INIST-CNRS ;Copyright American Thoracic Society Jun 1, 2014 ;Copyright © 2014 by the American Thoracic Society 2014 ;ISSN: 1073-449X ;EISSN: 1535-4970 ;DOI: 10.1164/rccm.201403-0535OE ;PMID: 24881936

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Title:
Resolution of Pulmonary Edema: Thirty Years of Progress
Author: MATTHAY, Michael A
Subjects: Alveolar Epithelial Cells - metabolism ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Body Fluids - metabolism ; Evidence-Based Medicine ; Humans ; Hypoxia - metabolism ; Intensive care medicine ; Medical sciences ; Occasional ; Pneumology ; Pulmonary Alveoli - metabolism ; Pulmonary Edema - diagnosis ; Pulmonary Edema - metabolism ; Receptors, Adrenergic - metabolism ; Receptors, Dopamine - metabolism ; Respiratory Distress Syndrome, Adult - diagnosis ; Respiratory Distress Syndrome, Adult - metabolism ; Respiratory system : syndromes and miscellaneous diseases ; Sodium-Potassium-Exchanging ATPase - metabolism ; Up-Regulation
Is Part Of: American journal of respiratory and critical care medicine, 2014-06, Vol.189 (11), p.1301-1308
Description: In the last 30 years, we have learned much about the molecular, cellular, and physiological mechanisms that regulate the resolution of pulmonary edema in both the normal and the injured lung. Although the physiological mechanisms responsible for the formation of pulmonary edema were identified by 1980, the mechanisms that explain the resolution of pulmonary edema were not well understood at that time. However, in the 1980s several investigators provided novel evidence that the primary mechanism for removal of alveolar edema fluid depended on active ion transport across the alveolar epithelium. Sodium enters through apical channels, primarily the epithelial sodium channel, and is pumped into the lung interstitium by basolaterally located Na/K-ATPase, thus creating a local osmotic gradient to reabsorb the water fraction of the edema fluid from the airspaces of the lungs. The resolution of alveolar edema across the normally tight epithelial barrier can be up-regulated by cyclic adenosine monophosphate (cAMP)-dependent mechanisms through adrenergic or dopamine receptor stimulation, and by several cAMP-independent mechanisms, including glucocorticoids, thyroid hormone, dopamine, and growth factors. Whereas resolution of alveolar edema in cardiogenic pulmonary edema can be rapid, the rate of edema resolution in most patients with acute respiratory distress syndrome (ARDS) is markedly impaired, a finding that correlates with higher mortality. Several mechanisms impair the resolution of alveolar edema in ARDS, including cell injury from unfavorable ventilator strategies or pathogens, hypoxia, cytokines, and oxidative stress. In patients with severe ARDS, alveolar epithelial cell death is a major mechanism that prevents the resolution of lung edema.
Publisher: New York, NY: American Thoracic Society
Language: English
Identifier: ISSN: 1073-449X
EISSN: 1535-4970
DOI: 10.1164/rccm.201403-0535OE
PMID: 24881936
Source: Geneva Foundation Free Medical Journals at publisher websites
AUTh Library subscriptions: ProQuest Central
MEDLINE
Alma/SFX Local Collection

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Resolution of Pulmonary Edema: Thirty Years of Progress

2015 INIST-CNRS ;Copyright American Thoracic Society Jun 1, 2014 ;Copyright © 2014 by the American Thoracic Society 2014 ;ISSN: 1073-449X ;EISSN: 1535-4970 ;DOI: 10.1164/rccm.201403-0535OE ;PMID: 24881936

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