Infiltration of activated neutrophils into the lung appears to be a key ele
ment in the severe lung injury that develops in animal models of acute lung
injury. Partial liquid ventilation with perflubron has been shown to ameli
orate tissue damage compared with conventional mechanical ventilation in ac
ute lung injury models. Pilot experiments indicated that indirect exposure
to perflubron could modulate the degree to which subsequent neutrophil bind
ing to endothelial cell monolayers was upregulated after lipopolysaccharide
activation. Endothelial cell monolayers preexposed to perflubron showed >4
0% reductions in the surface steady-state levels of E-selectin and intercel
lular adhesion molecule-1 achieved after proinflammatory activation (P < 0.
05), which correlated with a reduction in the real-time association constan
ts measured by biosensor techniques. These results indicate that direct con
tact with the perflubron liquid phase is not necessary to attenuate inflamm
atory responses. Rather, diffusion of perflubron from the alveolar space in
to the adjacent pulmonary vascular endothelial layer may modulate neutrophi
l adhesion and thereby reduce the rate of infiltration of activated neutrop
hils into the injured lung.