Objective: To examine whether chemically different perfluorochemical liquid
s (PFC) (perfluorodecalin [PFD]; perflubron [PFB]) induce inflammatory resp
onses in blood leukocytes.
Setting: University research laboratory.
Design: Whole blood from 12 healthy adults was incubated with increasing PF
C concentrations and/or bacterial lipopolysaccharide.
Measurements and Main Results: Adhesion molecules (CD62L, CD11b), reactive
oxygen species, and cytokine responses in resting and activated leukocyte s
ubtypes were studied. Scanning and transmission electron microscopies were
performed. At the highest concentrations, PFB stimulated a significant incr
ease in resting monocytic reactive oxygen species production; all types of
blood leukocytes were unresponsive to PFD. Neither PFB nor PFD changed CD62
L expression; PFB increased CD11b expression in monocytes and granulocytes.
PFD induced a small though significant increase in interleukin-8 secretion
. When simulating a condition in which patients with severe lung disease or
sepsis would be ventilated with PFC, neither PFB nor PFD plus lipopolysacc
haride stimulated tumor necrosis-alpha or interleukin-8 production above le
vels induced by lipopolysaccharide alone, but rather demonstrated a trend f
or decreased tumor necrosis factor-alpha production. Expression of CD11b an
d CD62L and the production of reactive oxygen species were not changed beyo
nd the levels induced by lipopolysaccharide alone. As a morphologic correla
te to the above proinflammatory changes, surface-bound blebs and intracellu
lar vacuoles were seen by electron microscopy.
Conclusions: At PFC concentrations comparable with those in blood during li
quid ventilation, PFC liquids did not induce variables associated with infl
ammation. In the presence of high PFC concentrations, simulating the condit
ion in which bronchoalveolar cells are exposed to PFC, monocytes may be ind
uced by PFB to produce reactive oxygen species, and blood leukocytes induce
d by PFB to express CD11b and by PFB) to secrete interleukin-8; the presenc
e of either PFC attenuated tumor necrosis factor-alpha production after lip
opolysaccharide stimulation.