Resolution of pulmonary edema. Thirty years of progress
Autor: | Michael A. Matthay |
---|---|
Rok vydání: | 2014 |
Předmět: |
Pulmonary and Respiratory Medicine
Epithelial sodium channel Pathology medicine.medical_specialty ARDS Alveolar Epithelium Dopamine alveolar epithelium Respiratory System Pulmonary Edema Critical Care and Intensive Care Medicine Medical and Health Sciences Receptors Dopamine chemistry.chemical_compound Rare Diseases Edema Receptors Medicine 2.1 Biological and endogenous factors Humans Cyclic adenosine monophosphate Aetiology Hypoxia Acute Respiratory Distress Syndrome Lung alveolar liquid clearance Respiratory Distress Syndrome Evidence-Based Medicine business.industry Hypoxia (medical) respiratory system Pulmonary edema medicine.disease Body Fluids Receptors Adrenergic Up-Regulation Pulmonary Alveoli Occasional Essay medicine.anatomical_structure chemistry acute lung injury Adrenergic Anesthesia Alveolar Epithelial Cells Respiratory medicine.symptom Sodium-Potassium-Exchanging ATPase business |
Zdroj: | American journal of respiratory and critical care medicine, vol 189, iss 11 |
ISSN: | 1535-4970 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |
načítá se...