The acute respiratory distress syndrome (ARDS) in adults is associated
with a wide variety of precipitating factors, often not directly invo
lving the lung, and has an associated mortality of 50-80%. ARDS is alm
ost invariably associated with sepsis, either as an initiating factor
or as a secondary complication, which increases the expression of a nu
mber of cytokines impacting upon several cellular systems. Specificall
y, activation of neutrophils sequestered in the pulmonary circulation
by this process, causes the release of free radicals and reactive oxyg
en species (ROS), increasingly regarded as key substances modulating t
he endothelial dysfunction and disruption responsible for the principa
l clinical manifestations of the syndrome. Here we discuss briefly the
pathophysiology of ARDS and its impact upon pulmonary vascular contro
l; the biological origins of free radicals and other ROS involved, the
mechanisms of their damaging effects, their contribution to the modif
ication of pulmonary vascular control mechanisms in lung injury and po
ssible therapeutic perspectives.