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2014 ; 189
(11
): 1301-8
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Resolution of pulmonary edema Thirty years of progress
#MMPMID24881936
Matthay MA
Am J Respir Crit Care Med
2014[Jun]; 189
(11
): 1301-8
PMID24881936
show ga
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.