Disparity in blood activation by two different heparin-coated cardiopulmonary bypass systems.
BACKGROUND
Several studies have indicated reduced "blood activation" in heparin-coated cardiopulmonary bypass systems. The present study compares the effect of two different heparin coatings on different blood activation indices.


METHODS
Low-risk patients (n = 40) were randomized to coronary artery bypass grafting using cardiopulmonary bypass with surfaces coated entirely by either the Duraflo II heparin coat or the Carmeda Biological Active Surface, or with identical uncoated equipment. In all cases, a standard systemic heparin dosage was used. Complement activation (C3 activation products C3bc and C3a and formation of fluid phase terminal SC5b-9 complement complex), neutrophil activation (lactoferrin and myeloperoxidase), and lytic inhibitors (vitronectin and clusterin) were quantified during cardiopulmonary bypass and 6 hours postoperatively.


RESULTS
Heparin coating by either method reduced the formation of terminal SC5b-9 complement complex and the release of lactoferrin and myeloperoxidase compared with uncoated systems. Lactoferrin and myeloperoxidase levels increased significantly during cardiopulmonary bypass in the Duraflo II group, whereas no significant increase was observed in the Carmeda Biological Active Surface group. The least formation of terminal SC5b-9 complement complex and neutrophil activation was observed with the Maxima Carmeda Biological Active Surface-coated equipment. The vitronectin and clusterin concentrations were significantly less reduced in the Duraflo II compared with the control group. This study underlines the importance of terminal SC5b-9 complement complex as a suitable marker in the evaluation of complement activation during cardiopulmonary bypass.


CONCLUSIONS
Both heparin coatings reduce blood activation, probably more so with Carmeda Biological Active Surface than with Duraflo II.
Department of Surgery, Institute for Experimental Research, Ullevaal Hospital, Oslo, Norway.
O
O
Moen
E
E
Fosse
V
V
Brockmeier
C
C
Andersson
T E
TE
Mollnes
K
K
Høgåsen
P
P
Venge
D000925:Anticoagulants; D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000295:instrumentation*; D051152:Clusterin; D003167:Complement Activation; D003169:Complement Inactivator Proteins / Q000032:analysis; D001026:Coronary Artery Bypass; D005260:Female; D006023:Glycoproteins / Q000097:blood; D006493:Heparin; D006801:Humans; D008297:Male; D018832:Molecular Chaperones; D018375:Neutrophil Activation; D013499:Surface Properties; D019096:Vitronectin / Q000097:blood
D000925:Anticoagulants; C495242:CLU protein, human; D051152:Clusterin; D003169:Complement Inactivator Proteins; D006023:Glycoproteins; D018832:Molecular Chaperones; D019096:Vitronectin; D006493:Heparin