A Heparin-Coated Circuit Reduces Complement Activation and the Release of Leukocyte Inflammatory Mediators During Extracorporeal Circulation in a Rabbit

Abstract

Heparin coating modifies complement activation during extracorporeal circulation much more effcclively than systemically administered heparin. This rabbit study was undertaken to address possible mechanisms responsible for this difference. We evaluated the effect of heparin coating on complement activation and subsequently the release of leukocyte inflammatory mediators during extracorporeal circulation through a simplified circuit. We found in the heparin-coated group a significantly reduced complement hemolytic activity (CH 50 ), remaining higher leukocyte numbers, significantly decreased release of -glucuronidase, and most strikingly a complete prevention of tumor necrosis factor (TNF) formation. The significantly reduced CH 50 activity in the heparin-coated groups indicates the reduction of one or more native classical complement products. This could be explained by the absorption of complement components by the circuit, which results in reduced activity of the complement cascade. We conclude therefore that heparin coating reduces complement activation and consequently reduces the release of leukocyte inflammatory mediators.