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Ann Thorac Surg 1994;58:421-424
© 1994 The Society of Thoracic Surgeons

Articles

Complement activation during cardiopulmonary bypass: Effects of immobilized heparin

Marcela Pekna, MD, PhD*, Leif Hagman, MD, Eric Haldén, MD, PhD, Ulf R. Nilsson, MD, PhD, Bo Nilsson, MD, PhD, Stefan Thelin, MD, PhD

Department of Clinical Immunology and Transfusion Medicine, Department of Thoracic and Cardiovascular Surgery and Department of Anesthesiology, University Hospital, Uppsala, Sweden

Accepted for publication December 3, 1993.

* Address reprint requests to Dr Pekna. Department of Medical Biochemistry, University of Göteborg, Medicinaregatan 9, S-41390. Göteborg, Sweden.

The role of complement in biocompatibility reactions and the correlation between complement activation during cardiopulmonary bypass (CPB) and postperfusion syndrome have inspired attempts to improve the biocompatibility of extracorporeal blood oxygenation devices. Here we assessed the effect of immobilized heparin on the generation of C3a and terminal complement complexes during CPB. Thirty patients undergoing aortocoronary bypass were randomized to CPB with either heparin-coated (Duraflo II; Bentley, Irvine, CA) or noncoated control membrane oxygenators (Univox; Bentley). A standard dose of heparin (300 IU/kg) was given to the control group while the heparin dose was reduced to 30% (100 IU/kg) in the heparin-coated group. Significantly lower levels of terminal complement complexes were detected in the heparin-coated group by the end of CPB. From 28 ± 5 AU/mL (heparin-coated group) and 26 ± 3 AU/mL (control group, mean ± standard error of the mean) the terminal complement complex levels increased to 391 ± 35 AU/mL and 602 ± 47 AU/mL, respectively (p < 0.002). This difference was still apparent 180 minutes after CPB. Although there was no difference in C3a levels between the two groups at the end of CPB, C3a levels were significantly lower in the heparin-coated group 30 minutes after CPB (194 ± 18 ng/mL and 307 ± 18 ng/mL in heparin-coated and control groups, respectively; p < 0.001). We conclude that the heparin-coated surface is more biocompatible with regard to complement activation than is the ordinary unmodifed surface in extracorporeal circuits.




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