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
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