Comparison of three oxygenator-coated and one total-circuit-coated extracorporeal devices.
The present study was designed to compare the biocompatibility of three cardiopulmonary bypass setups with different surface coatings, and to determine if coating of the whole circuit with one of the coatings was more beneficial than coating of the oxygenator only. Extracorporeal devices entirely coated with synthetic polymers (Avecor, n = 6) were compared to oxygenators coated with synthetic polymers (Avecor, n = 6), end-point, covalently attached heparin (CBAS, n = 6) or absorbed heparin (Duraflo 2, n = 6) in an in vitro model of a heart lung machine. The circuits were primed with fresh human whole blood and Ringer's acetate and recirculated at 4 l/min at 30 degrees C for 2 h. Test samples were obtained at regular intervals and analysed for myeloperoxidase (MPO), platelet counts, beta-thromboglobulin, heparin, prothrombin fragment 1+2, plasmin anti-plasmin complexes, and complement activation products. The mean MPO concentrations increased in the Avecor-coated oxygenator group (AV) from 247 at the start to 671 microg/l at the termination of the experiments, in the Avecor-coated total circuit group (AV-T) from 116 to 288 microg/l, in the Duraflo 2 coated oxygenator group (DU) from 160 to 332 microg/l, and in the CBAS-coated oxygenator (CA) group from 172 to 311 microg/l. The MPO concentrations increased significantly in all groups (p < 0.03). The increase in group A was significantly higher than in the other three groups (p = 0.007). The mean platelet counts decreased in the Avecor-coated total circuit group from 117 at start to 99 x 10(9)/l at termination of the experiments, in the Avecor-coated oxygenator group from 119 to 103 x 10(9)/l, in the Duraflo 2 group from 96 to 86 x 10(9)/l, and in the CBAS group from 132 to 123 x 10(9)/l. The platelet counts decreased significantly in all groups (p < 0.01), but the intergroup differences were not significant (p = 0.15). The mean beta-thromboglobulin concentrations increased in the Avecor-coated total circuit group from 193 at the start to 754 ng/ml at the termination of the experiments, in the Avecor-coated oxygenator group from 474 to 1654 ng/l, in the Duraflo 2 group from 496 to 1280 ng/l, and in the CBAS group from 418 to 747 ng/l. The beta-thromboglobulin increase was significant in each group (p < 0.01), but not between the groups (p = 0.49). The mean heparin concentrations in the Duraflo 2 group increased from 2460 at the start to 2897 IU/l at termination of the experiments, in the CBAS group from 2468 to 2518 IU/l. In the Avecor-coated oxygenator group heparin concentrations decreased from 2010 to 1968 IU/l, and in the Avecor-coated total circuit group from 2002 to 1927 IU/l. The differences in heparin concentrations were significant between the Duraflo 2 group and the other groups (p < 0.05). The mean prothrombin fragment 1+2 concentrations increased in the CBAS group from 0.4 at the start to 2.1 nmol/l at the end of the experiments, in the Avecor-coated oxygenator group from 0.4 to 0.6 nmol/l, in the Avecor-coated total circuit group from 0.3 to 0.4 nmol/l, and in the Duraflo 2 group from 1.2 to 1.3 nmol/l. The prothrombin fragment 1+2 increase was significant in all groups (p < 0.05), but there were no significant intergroup differences (p = 0.54). There were no significant differences at the termination of the experiments among the four groups regarding complement activation as measured by C3 activation products and the terminal complement complex. In the present in vitro model of a heart-lung machine, none of the three specific setups with different coatings was superior with regard to all test parameters. The CBAS group generated the highest levels of prothrombin fragment 1+2 formation, but least complement activation. The increasing plasma heparin concentrations in the Duraflo 2 group indicated more unstable heparin bonding. The Avecor-coated total circuit group were superior to the Avecor-coated oxygenator group regarding plasma concentrations of MPO, but not compa
Baksaas
S T
ST
Department of Surgery A, The National Hospital, University of Oslo, Norway.
Videm
V
V
Pedersen
T
T
Karlsen
H
H
Mollnes
T E
TE
Brosstad
F
F
Svennevig
J L
JL
D000933:Antifibrinolytic Agents; D001672:Biocompatible Materials; D003179:Complement C3b / Q000032:analysis; D015938:Complement Membrane Attack Complex / Q000032:analysis; D004867:Equipment Design; D004864:Equipment and Supplies; D005112:Extracorporeal Circulation / Q000295:instrumentation*; D005341:Fibrinolysin / Q000032:analysis; D006493:Heparin / Q000097:blood; D006801:Humans; D007958:Leukocyte Count; D010106:Oxygenators; D010446:Peptide Fragments / Q000032:analysis; D009195:Peroxidase / Q000097:blood; D010976:Platelet Count; D011516:Prothrombin / Q000032:analysis; D012828:Silicones; D013499:Surface Properties; D000979:alpha-2-Antiplasmin / Q000032:analysis; D001620:beta-Thromboglobulin / Q000032:analysis
D000933:Antifibrinolytic Agents; D001672:Biocompatible Materials; D015938:Complement Membrane Attack Complex; D010446:Peptide Fragments; D012828:Silicones; D000979:alpha-2-Antiplasmin; D001620:beta-Thromboglobulin; C037742:plasmin-plasmin inhibitor complex; C045879:prothrombin fragment 1.2; D003179:Complement C3b; D011516:Prothrombin; D006493:Heparin; D009195:Peroxidase; D005341:Fibrinolysin