In vitro evaluation of new surface coatings for extracorporeal circulation

Cardiopulmonary bypass (CPB) exposes blood to large, foreign surfaces. This exposure may activate the cellular and humoral inflammatory systems, resul ting in inflammatory reactions and organ dysfunction. Coating the inner sur faces of the bypass circuit may help alleviate these side-effects. The obje ctive of this study was to determine the influence of two new surface treat ments on blood cell and complement activation. Oxygenator and tubing sets coated with synthetic polymers (n = 7) or hepari n (n = 7) were compared to uncoated sets (n = 7) in an in vitro model of CP B. The circuits were run at 4 I/min and recirculated for 120 min. The infla mmatory response was assessed at regular intervals by platelet counts, and activation of complement, leucocytes and platelets. We found that the median platelet counts decreased from 127 to 122 x 10(9)/ l (not significant, NS) in the synthetic polymer sets, from 96 to 88 x 10(9 )/l (NS) in the heparin-coated sets, and from 93 to 54 x 10(9)/l (p < 0.01) in the uncoated sets after 2 h of recirculation. There were significant di fferences in platelet counts between the coated sets and the uncoated set a t end of experiments (p < 0.05). Beta-thromboglobulin (BTG) concentrations increased in the synthetic polymer sets from 166 to 352 ng/ml (p < 0.01), i n the heparin coated sets from 336 to 1168 ng/ml (p < 0.01), and in the unc oated sets from 301 to 3149 ng/ml (p < 0.01) after 2 h of recirculation. Th e differences in BTG at termination of the experiments were significant amo ng all three sets (p < 0.05). Myeloperoxidase (MPO) concentrations in the s ynthetic polymer sets increased from 63 to 86 mu g/l (p < 0.01), in the hep arin-coated sets from 90 to 208 mu g/l (p < 0.01), and in the uncoated sets from 122 to 513 mu g/l (p < 0.01) after 2 h of recirculation. The differen ces in MPO at termination of the experiments were significant among ail thr ee groups (p < 0.01). There were no significant differences at termination of the experiments among the three sets regarding complement activation as measured by C3 activation products and the terminal complement complex. We conclude that in the current in vitro model of a CPB circuit, the synthe tic polymer coating and the heparin coating caused significantly less plate let loss and granulocyte and platelet activation than the uncoated surface (p < 0.05). The synthetic polymer coating caused significantly less granulo cyte and platelet activation than the heparin coating (p < 0.05). There was moderate complement activation within each group, but no significant diffe rences among the three groups.