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J Thorac Cardiovasc Surg 1996;111:451-459
© 1996 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Sheffield, Cardiff, London, and Harlow, Great Britain
Supported in part by research grants from the Richard Hall Trust, the Child Health Research Appeal Trust, and SmithKline Beecham Pharmaceuticals.
Received for publication Sept. 2, 1994. Accepted for publication May 9, 1995. Address for reprints: Adam Finn, MA, PhD, MRCP(UK), Department of Pediatrics, Children's Hospital, Sheffield, S10 2TH, United Kingdom.
Abstract
The inflammatory response to cardiopulmonary bypass includes activation of complement and induction of several neutrophil activation pathways. A recombinant soluble form of complement receptor 1 was used as a specific inhibitor of complement activation in simulated cardiopulmonary bypass circuits. Substantial complement activation was observed in these circuits with progressive accumulation of both plasma C3a and terminal complement complex. Soluble complement receptor 1 resulted in a significant reduction in C3a levels (p < 0.01) but did not inhibit terminal complement complex generation. A marked rise in neutrophil CD11b/CD18 expression, simultaneous loss of L-selectin expression, and a progressive accumulation of plasma elastase–
1-antitrypsin occurred and were not affected by soluble complement receptor. However, generation of interleukin-8 in the circuits was inhibited (p < 0.05) by pretreatment with soluble complement receptor. These data suggest that changes in neutrophil activation seen during cardiopulmonary bypass may not be induced directly by anaphylatoxin generation. (J THORACCARDIOVASCSURG1996;111:451-9)
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