Heparin-coated cardiopulmonary bypass equipment. II. Mechanisms for reduced complement activation in vivo

Citation
V. Videm et al., Heparin-coated cardiopulmonary bypass equipment. II. Mechanisms for reduced complement activation in vivo, J THOR SURG, 117(4), 1999, pp. 803-809
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
ISSN journal
00225223 → ACNP
Volume
117
Issue
4
Year of publication
1999
Pages
803 - 809
Database
ISI
SICI code
0022-5223(199904)117:4<803:HCBEIM>2.0.ZU;2-S
Abstract
Objective: Our objective was to study mechanisms for reduced complement act ivation by heparin coating of cardiopulmonary bypass equipment in clinical heart surgery, Methods: Adults undergoing elective coronary artery bypass g rafting were randomized to cardiopulmonary bypass with Duraflo II heparin-c oated (n = 15) or uncoated (n = 14) sets (Duraflo coating surface; Baxter I nternational, Inc, Deerfield, Ill), Blood samples were analyzed with the us e 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 w as activated during bypass, and increases in C1rs-C1 inhibitor complexes we re larger with heparin coating (P = .03). C4bc increased after administrati on of protamine, without intergroup differences (P = .69). Bb (P = .22) and C5a-desArg (P = .13) tended to increase less with heparin coating. Formati on of C3bc (P = .03) and the terminal complement complex (P < .01) was sign ificantly reduced with heparin coating. C5a-desArg increased 2-fold during bypass, whereas the terminal complement complex increased 10- to 20-fold, M aximal terminal complement complex concentrations were significantly correl ated to maximal Bb and C3bc (R = 0.6, P < .001), but not to C1rs-C1 inhibit or complexes or C4bc (R < 0.05, P > .8). Conclusions: C1 activation during bypass was increased by heparin coating, but further classical pathway acti vation was held in check until administration of protamine, Heparin coating significantly inhibited C3bc and terminal complement complex formation. Te rminal complement complex concentrations were related to alternative pathwa y activation and may be useful for evaluation of differences in bypass circ uitry. Increases and intergroup differences in terminal complement complex concentrations were much larger than those in C5a-desArg.