Abstract
The complement system is often most noted for its ability to lyse certain microorganisms. In the intact organism, however, its role in initiating inflammation is probably of greater importance. Being able to react within minutes, the complement system helps alert the other defense systems to threats of damage, whether caused by microorganisms or physiochemical factors–or the artificial surfaces of an extracorporeal circuit. Its central role in the inflammatory response after cardiopulmonary bypass (CPB) has been acknowledged since the early 1980s. Consequently, when heparin-coated CPB equipment became commercially available and was shown to dramatically reduce complement activation, there were great hopes that the risks of postoperative complications would also drop substantially. Why did this to a large extent turn out not to be the case?
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