EFFECTS OF INHIBITION OF COMPLEMENT ACTIVATION USING RECOMBINANT SOLUBLE COMPLEMENT RECEPTOR-1 ON NEUTROPHIL CD11B CD18 AND L-SELECTIN EXPRESSION AND RELEASE OF INTERLEUKIN-8 AND ELASTASE IN SIMULATED CARDIOPULMONARY BYPASS/

The inflammatory response to cardiopulmonary bypass includes activatio n of complement and induction of several neutrophil activation pathway s, A recombinant soluble form of complement receptor 1 was used as a s pecific inhibitor of complement activation in simulated cardiopulmonar y bypass circuits. Substantial complement activation was observed in t hese circuits with progressive accumulation of both plasma C3a and ter minal complement complex, Soluble complement receptor 1 resulted in a significant reduction in C3a levels (p < 0.01) but did not inhibit ter minal complement complex generation, A marked rise in neutrophil CD11b /CD18 expression, simultaneous loss of L-selectin expression, and a pr ogressive accumulation of plasma elastase-alpha(1)-antitrypsin occurre d and were not affected by soluble complement receptor. However, gener ation of interleukin-8 in the circuits was inhibited (p < 0.05) by pre treatment with soluble complement receptor. These data suggest that ch anges in neutrophil activation seen during cardiopulmonary bypass may not be induced directly by anaphylatoxin generation.