Effect of complement inhibition and heparin coating on artificial surface–induced leukocyte and platelet activation Knut Tore Lappegård, MD, Michael.

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Effect of complement inhibition and heparin coating on artificial surface–induced leukocyte and platelet activation Knut Tore Lappegård, MD, Michael Fung, PhD, Grethe Bergseth, BS, Johan Riesenfeld, PhD, John D Lambris, PhD, Vibeke Videm, MD, PhD, Tom Eirik Mollnes, MD, PhD The Annals of Thoracic Surgery Volume 77, Issue 3, Pages 932-941 (March 2004) DOI: 10.1016/S0003-4975(03)01519-4

Fig 1 The complement system. The three initial and the terminal activation pathways of complement are schematically illustrated with the activation products measured in the present study in boxes. C1rs–C1-inhibitor (C1rs-C1inh) complexes are specific for the classic pathway, C4bc is generated both from the classic and the lectin pathways, C3bBbP is specific for the alternative pathway, C3bc is generated from any of the three initial pathways, and the terminal SC5b-9 complement complex (TCC) is the final activation product of the terminal pathway. (MASP = MBL-associated serine protease; MBL = mannose-binding lectin.) The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 2 Activation of complement by uncoated (PVC) and heparin-coated polyvinyl chloride (H-PVC), and the effect of specific complement inhibitors. Human whole blood with or without complement inhibitors was circulated for 15 minutes in segments of tubing rotated as closed loops, whereupon complement activation was determined as the plasma concentrations of C3bBbP (left), terminal SC5b-9 complement complex (TCC; middle), and C1rs–C1-inhibitor complexes (right). Inhibitors were added to blood circulated in uncoated PVC tubing only. Data are expressed as percent of baseline (preincubation value) set as 100%. Median, 25th to 75th percentiles, and total range are shown; n = 6 for each inhibitor, n = 18 for PVC and H-PVC. *p < 0.05 versus PVC. (Anti-C5 = anti-C5 [50 μg/mL]; Anti-D = anti-factor D [10 μg/mL]; B = baseline; Comp = compstatin [100 μmol/L]; TCC = terminal complement complex.) The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 3 Expression of CD11b on leukocytes in blood exposed to uncoated (PVC) and heparin-coated polyvinyl chloride (H-PVC), and the effect of complement inhibitors. Human whole blood with or without complement inhibitors was circulated for 15 minutes in tubing loops, followed by measurement of CD11b expression on granulocytes (left) and monocytes (right) by flow cytometry. Inhibitors were added to blood circulated in uncoated polyvinyl chloride tubing only. Data are given as percent of baseline (B) median fluorescent intensity, which is set as 100%. n = 6 for each inhibitor; n = 24 for PVC and H-PVC. *p < 0.05 versus PVC. (C5aRA = C5a receptor antagonist [5 μmol/L]; Comp = compstatin [100 μmol/L].) The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 4 Formation of leukocyte–platelet conjugates in blood exposed to uncoated (PVC) and heparin-coated polyvinyl chloride (H-PVC), and the effect of complement inhibitors. Human whole blood with or without complement inhibitors was circulated for 15 minutes in tubing loops, after which granulocyte-platelet (left) and monocyte-platelet (right) conjugates were quantified by flow cytometry. Inhibitors were added to blood circulated in uncoated polyvinyl chloride tubing only. Data are given as percent of baseline (B) median fluorescence intensity, which is set as 100%. n = 6 for each inhibitor, n = 24 for PVC and H-PVC. *p < 0.05 versus PVC. (Comp = compstatin [100 μmol/L].) The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 5 Platelet granula release in blood exposed to uncoated (PVC) and heparin-coated polyvinyl chloride (H-PVC), and the effect of complement inhibitors. Human whole blood with or without complement inhibitors was circulated for 5 minutes in tubing loops, followed by measurement of thrombospondin in plasma. Inhibitors were added to blood circulated in uncoated polyvinyl chloride tubing only. Median and range of three experiments, expressed as percent of baseline (B) set as 100%, are shown. (Comp = compstatin [100 μmol/L].) The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 6 Neutrophil degranulation in blood exposed to uncoated and heparin-coated polyvinyl chloride. Human whole blood was circulated for 1, 2, or 4 hours in loops of uncoated (closed squares) and heparin-coated polyvinyl chloride (open squares), followed by quantification of plasma myeloperoxidase (left) and lactoferrin (right). Data are given as percent of baseline (B) value set as 100%. Median and range of three experiments are shown. The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)

Fig 7 Effect of the heparin surface on complement activation in the fluid phase. Human whole blood with or without addition of complement activating heat-aggregated immunoglobulin (HAIGG) was circulated for 1 hour in loops of uncoated (PVC) or heparin-coated polyvinyl chloride (H-PVC) tubing. The resulting plasma concentrations of C1rs–C1-inhibitor complexes (left) and terminal SC5b-9 complement complex (TCC; right) were quantified. One representative result from three experiments, expressed as percent of baseline (B) value set as 100%, is shown. The Annals of Thoracic Surgery 2004 77, 932-941DOI: (10.1016/S0003-4975(03)01519-4)