We have examined whether propofol activates complement. In the first study,
blood was mix-ed with saline, propofol or the lipid solvent for propofol,
and the activated complement 3 (C3a) and 4 (C4a) concentrations in the supe
rnatant were assayed. In the second study, blood and propofol were mixed wi
th various levels of nafamostat mesilate (anti-complement agent) up to 0.3
mmol/l and the C3a was assayed. In the third study, the time course of plas
ma C3a concentration in patients during propofol anaesthesia was examined T
he results showed that the lipid solvent activated complement and produced
similar levels of C3a to propofol, probably via both the classical and alte
r-native pathways. This activation was not inhibited by ally of the nafamos
tat concentrations used. There was no significant change in plasma C3a conc
entration during propofol anaesthesia. These results suggest that C3a is ge
nerated by the lipid solvent, but its accumulation during propofol anaesthe
sia is minimal.