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J Thorac Cardiovasc Surg 1999;117:803-809
© 1999 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

HEPARIN-COATED CARDIOPULMONARY BYPASS EQUIPMENT. II. MECHANISMS FOR REDUCED COMPLEMENT ACTIVATION IN VIVO

From the Department of Surgery A, Institute for Surgical Research, Department of Anaesthesiology, and Department of Clinical Chemistry, The National Hospital, Oslo University, Oslo; Department of Immunology and Blood Bank and Department of Microbiology, The Regional Hospital, Norwegian University of Science and Technology, Trondheim; and Department of Immunology and Transfusion Medicine, Nordland Central Hospital, Bodø, University of Tromsø, Tromsø, Norway.

The study was supported by The Norwegian Research Council, Medical Innovation at The National Hospital, and the Norwegian Council on Cardiovascular Research.

Received for publication March 10, 1998. Revisions requested July 9, 1998. Revisions received Oct 26, 1998. Accepted for publication Nov 6, 1998. Address for reprints: Vibeke Videm, MD, PhD, Department of Immunology and Blood Bank, The Regional Hospital, N-7006 Trondheim, Norway.

Objective: Our objective was to study mechanisms for reduced complement activation by heparin coating of cardiopulmonary bypass equipment in clinical heart surgery.
Methods: Adults undergoing elective coronary artery bypass grafting were randomized to cardiopulmonary bypass with Duraflo II heparin-coated (n = 15) or uncoated (n = 14) sets (Duraflo coating surface; Baxter International, Inc, Deerfield, Ill). Blood samples were analyzed with the use of enzyme immunoassays for C1rs-C1 inhibitor complexes and the activation products Bb, C4bc, C3bc, C5a-desArg, and the terminal complement complex. Data were compared by repeated-measures analysis of variance.
Results: C1 was activated during bypass, and increases in C1rs-C1 inhibitor complexes were larger with heparin coating (P = .03). C4bc increased after administration of protamine, without intergroup differences (P = .69). Bb (P = .22) and C5a-desArg (P = .13) tended to increase less with heparin coating. Formation of C3bc (P = .03) and the terminal complement complex (P < .01) was significantly reduced with heparin coating. C5a-desArg increased 2-fold during bypass, whereas the terminal complement complex increased 10- to 20-fold. Maximal terminal complement complex concentrations were significantly correlated to maximal Bb and C3bc (R = 0.6, P < .001), but not to C1rs-C1 inhibitor complexes or C4bc (R < 0.05, P > .8).
Conclusions: C1 activation during bypass was increased by heparin coating, but further classical pathway activation was held in check until administration of protamine. Heparin coating significantly inhibited C3bc and terminal complement complex formation. Terminal complement complex concentrations were related to alternative pathway activation and may be useful for evaluation of differences in bypass circuitry. Increases and intergroup differences in terminal complement complex concentrations were much larger than those in C5a-desArg.

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