Endothelial injury consequent upon widespread humoral and cellular act
ivation is probably a major contributor to the phenomenon of cardiopul
monary bypass-induced organ dysfunction. This article reviews some of
the mechanisms by which complement and neutrophil activation and inter
leukin-8 may be involved in this inflammatory response. In a model con
sisting of a simulated extracorporeal circulation we were able to demo
nstrate complement activation, profound and specific changes in neutro
phil adhesion molecule expression, and interleukin-8 generation. The i
mportance of these changes and their potential interactions are discus
sed.