Therapeutic potential of complement inhibitors in myocardial ischaemia

Bibliography

• YASOJIMA K, KILGORE KS, WASHINGTON RA, LUCCHESI BR, MCGEER PL: Complement gene expression by rabbit heart: upregulation by ischemia and reperfu-sion. Circ. Res. (1998) 82(10:1224–1230.
   PubMed Web of Science ®Google Scholar
• ••This study challenges the previous assumption that injuriouscomplement contributing to reperfusion injury is derived solely from plasma.
   Google Scholar
• YASOJIMA K, SCHWAB C, MCGEER EG, MCGEER PL: Human heart generates complement proteins that are upregulated and activated after myocardial infarction. Circ. Res. (1998) 83(8):860–869.
   PubMed Web of Science ®Google Scholar
• ROSS SC, DENSEN P: Complement deficiency states and infection: epidemiology, pathogenesis and consequences of Neisserial and other infections in an immune deficiency. Medicine (1984) 63(5)243–273.
   Google Scholar
• WHALEY K, SCHWAEBLE W: Complement and comple-ment deficiencies. Sem. Liver Disease. (1 9 9 7) 17(0297–310.
   Google Scholar
• ESSER AF: The membrane attack complex of comple-ment. Assembly structure and cytotoxic activity. Toxicology (1991) 87(1-3):229–247.
   Google Scholar
• PAPADIMITRIOU JC, RAMM LE, DRACHENBERG CB, TRUMP BF, SHIN ML: Quantitative analysis of adenine nucleotides during the prelytic phase of cell death mediated by C5b-9. j Immunol (1991) 147(1):212–217.
   PubMed Web of Science ®Google Scholar
• PINCKARD RN, OLSON MS, KELLEY RE et al.: Antibody-independent activation of human Cl after interaction with heart subcellular membranes. J. Immunol. (1972) 110(5)1376–1382.
   Google Scholar
• PINCKARD RN, OLSON MS, GICLAS PC, TERRY R, BOYER JT, O'ROURKE RA: Consumption of classical comple-ment components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. Clin. Invest. (1975) 56(3):740–750.
   Google Scholar
• COLLARD CD, VAKEVA A, BUKUSOGLU C et al.: Reoxygenation of hypoxic human umbilical vein endothelial cells activates the classic complement pathway. Circulation (1997) 96 (1) :326–333.
   PubMed Web of Science ®Google Scholar
• SATO T, ENDO Y, MATSUSHITA M, FUJITA T: Molecular characterization of a novel serine protease involved in activation of the complement system by mannose-binding protein. Int. Immunol. (1994) 6(4):665–669.
   PubMed Web of Science ®Google Scholar
• MATSUSHITA M: The lectin pathway of the complement system. Microbiol Immunol. (1996) 40(12):887–893.
   PubMed Web of Science ®Google Scholar
• THIEL S, VORUP-JENSEN T, STOVER CM et al.: A second serine protease associated with mannan-binding lectin that activates complement. Nature (1997) 386(6624):506–510.
   PubMed Web of Science ®Google Scholar
• DREYER WJ, MICHAEL LH, NGUYEN T et al.: Kinetics of C5a release in cardiac lymph of dogs experiencing coronary artery ischemia-reperfusion injury. Circ. Res. (1992) 71(6):1518–1524.
   PubMed Web of Science ®Google Scholar
• AMSTERDAM EA, STAHL GL, PAN H-L, RENDIG SV, FLETCHER MP, LONGHURST JC: Limitation of reperfu-sion injury by a monoclonal antibody to C5a during myocardial infarction in pigs. Am. J. Physiol (1995) 268:448-457 (Heart Circ. Physiol. 37).
   Google Scholar
• •The importance of C5a-mediated injury in the reperfused myocardium is revealed as anti-05a antibodies attenuate tissue damage without hindering full complement activation.
   Google Scholar
• BIRDSALL HH, GREEN DM, TRIAL J et al.: Complement C5a, TGF-61 and MCP-1 in sequence, induce migration of monocytes into ischemic canine myocardium within the first one to five hours after reperfusion. Circulation (1997) 95(3):684–692.
   PubMed Web of Science ®Google Scholar
• FITCH JC, ROLLINS S, MATIS L et al.: Pharmacology and biological efficacy of a recombinant, humanized, single-chain antibody C5 complement inhibitor in patients undergoing coronary artery bypass graft surgery with cardiopulmonary bypass. Circulation (1999) 100(25)2499–2506.
   Google Scholar
• ••Anti-05 therapy is shown to protect the brain as well as theheart in this clinical study.
   Google Scholar
• STEPHENS L, EGUINO A, COREY S, JACKSON T, HAWKINS PT: Receptor stimulated accumulation of phosphatidy-linositol (3, 4, 5)-triphosphate by G-protein mediated pathways in human myeloid derived cells. EMBO (1993) 12(6):2256–2273.
   Google Scholar
• CHENOWETH DE, HUGLI TE: Demonstration of specific C5a receptor on intact human polymorphonuclear leukocytes. Proc. Natl. Acad. Sci. USA (1 9 7 8) 75 (8):3943–3947.
   Google Scholar
• HUEY R, HUGLI TE: Characterization of a C5a receptor on human polymorphonuclear leukocytes (PMN). J. Immunol. (1985) 135(3):2063–2068.
   PubMed Web of Science ®Google Scholar
• FOREMAN KE, VAPORCIYAN AA, BONISH BK et al.: C5a induced expression of P-selectin in endothelial cells. (1994) J. Clin. Invest. 94(3):1147–1155.
   Google Scholar
• WETSEL RA: Expression of the complement C5a anaphylatoxin receptor (C5aR) on non-myeloid cells. Immunol. Lett. (1995) 44(2–3)183–187.
   Google Scholar
• OSAKA H, MCGINTY A, HOPKEN UE, LU B, GERARD C, PASINETTI GM: Expression of C5a receptor in mouse brain: role in signal transduction and neurodegenera-tion. Neuroscience (1998) 88 (4):1073–1082.
   Web of Science ®Google Scholar
• WARD PA, NEWMAN LJ: A neutrophil chemotactic factor from human C'5. J. Immunol. (1 9 6 9) 102(1)693–709.
   Google Scholar
• BECKER EL, SHOWELL HJ, HENSON PK, HSU LS: The ability of chemotactic factors to induce lysosomal enzyme release. I. The characteristics of the release and the importance of surfaces and the relation of enzyme release to chemotactic responsiveness. J. Immunol. (1974) 1 12 (6):2047–2054.
   Google Scholar
• BECKER EL, SHOWELL HJ: The ability of chemotactic factors to induce lysosomal enzyme release. II. The mechanism of release. J. Immunol. (1 9 7 4) 1 12(6):2055–2062.
   Google Scholar
• GOLDSTEIN I, HOFFSTEIN S, GALLIN J, WEISSMANN G: Mechanisms of lysosomal enzyme release from human leukocytes: microtubule assembly and membrane fusion induced by a component of comple-ment. Proc. Natl. Acad. Sci. USA (1973) 70(102916–2920.
   Web of Science ®Google Scholar
• ENGLER RL, SCHMID-SCHONBEIN GW, PAVELEC RS: Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am. J. Pathol. (1983) 111(0:98–111.
   PubMed Web of Science ®Google Scholar
• MULLANE KM, READ N, SALMON JA, MONCADA S: Role of leukocytes in acute myocardial infarction in anesthe-tized dogs: relationship to myocardial salvage by anti-inflammatory drugs. J. Pharmacol. Exp. Ther. (1984) 228 (2):510–522.
   PubMed Web of Science ®Google Scholar
• MEHTA JL, NICHOLS WW, MEHTA P: Neutrophils as potential participants in acute myocardial ischemia: relevance to reperfusion. J. Am. Coll. Cardiol (1988) 11(6):1309–1316.
   PubMed Web of Science ®Google Scholar
• LEY K, BULLARD D, ARBONES ML et al.: Sequential contribution of L- and P-selectin to leukocyte rolling in vivo. J. Exp. Med. (1995) 181(2):669–675.
   PubMed Web of Science ®Google Scholar
• HUGLI TE, MOLLER-EBERHARD HJ: Anaphylatoxins: C3a and C5a. Adv. Immunol. (1978) 26:1–53.
   PubMedGoogle Scholar
• HUGLI TE: Structure and function of the anaphyla-toxins. Springer Semin. Immunopathol. 7(2–3) :193–219.
   Google Scholar
• GOLDSTEIN IM: Complement: biologically active products. In: Inflammation: Basic Principles and Clinical Correlates. Gallin JI, Goldstein IM, Synderman R (Eds.), Raven Press, New York, USA (1988):55–74.
   Google Scholar
• HOSTETTER MK: C3 and C4 as opsonins in natural immunity. In: Humoral Factors. Sim E (Ed.), Oxford University Press, New York, USA (1993) :177–208.
   Google Scholar
• VIK DP, FEARON DT: Neutrophils express a receptor for iC3b, C3dg and C3d that is distinct from CR1, CR2 and CR3. J. Immunol (1985) 134 (4) :2571–2579.
   PubMed Web of Science ®Google Scholar
• YANCEY KB, O'SHEA J, CHUSED T et al.: Human C5a modulates monocyte Fe and C3 receptor expression. J. Immunol (1985) 135(0:465–470.
   Google Scholar
• KILGORE KS, MILLER BF, FLORY CM, EVANS VM, WARREN JS: The membrane attack complex of complement induces monocyte chemoattractant protein-1 and interkeukin-8 secretion from human umbilical vein endothelial cells. Am. J. Pathol. (1996) 149 (3) :953–961.
   PubMed Web of Science ®Google Scholar
• KILGORE KS, SHEN J, MILLER BF, WARD PA, WARREN JS: Enhancement by the complement membrane attack complex of tumor necrosis factor-a-induced endothe-lial cell expression of ICAM-1 and E-selectin. J. Immunol. (1995) 155(3):1434–1441.
   PubMed Web of Science ®Google Scholar
• HATTORI R, HAMILTON KK, McEVER RP, SIMS PJ: Complement proteins C5b-9 induce secretion of high molecular weight multimers of endothelial von Willenbrand factor and translocation of granule membrane protein GMP-140 to the cell surface. J. Biol. Chem (1989) 264(15):9053–9060.
   PubMed Web of Science ®Google Scholar
• WERNS SW, LUCCHESI BR: Free radicals and ischemic tissue injury. Trends Pharmacol. Sci. (1990) 11 (4) :161–166.
   PubMed Web of Science ®Google Scholar
• ADLER S, BAKER PJ, JOHNSON RJ, OCHI RF, PRITZL P, COUSER WG: Complement membrane attack complex stimulates production of reactive oxygen metabolites by cultured rat mesangial cells. J. Clin. Invest. (1986) 77(3):762–767.
   PubMed Web of Science ®Google Scholar
• HANSCH GM, SEITZ M, BETZ M: Effect of the late comple-ment components C5b-9 on human monocytes: release of prostanoids, oxygen radical and of a factor inducing cell proliferation. Int. Arch. Allergy Appl. Immunol. (1987) 82(3-4):317–321.
   PubMedGoogle Scholar
• REITER Y, CIOBOTARIU A, FISHELSON Z: Sublyticcomplement attack protects tumor cells from lytic doses of antibody and complement. Eur. I Immunol (1992) 22(5):1207–1213.
   PubMed Web of Science ®Google Scholar
• MARCHBANK KJ, VAN DEN BERG CW, MORGAN BP: Mechanisms of complement resistance induced by non-lethal complement attack and by growth arrest. Immunology (1997) 90 (4) :647–653.
   PubMed Web of Science ®Google Scholar
• NICULESCU F, RUS H, SHIN ML: Receptor-independentactivation of guanine nucleotide-binding regulatory proteins by terminal complement complexes. J. Biol. Chem. (1994) 269(6):4417–4423.
   PubMed Web of Science ®Google Scholar
• CARNEY DF, LANG TJ, SHIN ML: Multiple signal messen-gers generated by terminal complement complexes and their role in terminal complement complex elimination. J. Immunol. (1990) 145(2):623–629.
   PubMed Web of Science ®Google Scholar
• •Examines the ability of the terminal components and the MAC to activate PKC and alter intracellular cAMP levels, giving evidence that these channels can act as signalling devices.
   Google Scholar
• MORGAN BP, CAMPBELL AK: A recovery of human polymorphonuclear leukocytes from sublytic comple-ment attack is mediated by changes in intracellular free calcium. Biochem. J. (1985) 231(0:205–208.
   PubMed Web of Science ®Google Scholar
• CARNEY DF, HAMMER CH, SHIN ML: Elimination of terminal complement complexes in the plasma membrane of nucleated cells: influence of extracel-lular Ca2+ and association with cellular Ca2+. J. Immunol. (1986) 137(0:263–270.
   PubMed Web of Science ®Google Scholar
• TEDESCO F, PAUSA M, NARDON E, INTRONA M, MANTOVANI A, DOBRINA A: The cytolytically inactive terminal complement complex activates endothelial cells to express adhesion molecules and tissue factor procoagulant activity. J. Exp. Med. (1997) 185(9):1619–1627.
   PubMed Web of Science ®Google Scholar
• •Aside from causing cell lysis, complement elicits a variety of cellular responses that promote tissue injury as illustrated in this study.
   Google Scholar
• HILL JH, WARD PA: The phlogistic role of C3 leukotactic fragments on myocardial infarcts of rats. J. Exp. Med. (1971) 133(4):885–900.
   PubMed Web of Science ®Google Scholar
• SCHAFER H, MATHEY D, HUGO F, BHAKDI S: Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. 1 Immunol (1986) 137(6):19454–1949.
   Google Scholar
• ••Histological evidence is presented, clearly demonstratingthe presence of the MAC in infarcted tissue and its virtual absence in neighbouring normal tissue.
   Google Scholar
• MATHEY D, SCHOFER J, SCHAFER HJ et al: Early accumulation of the terminal complement-complex in the ischaemic myocardium after reperfusion. Eur. Heart J. (1994) 15(3):418–423.
   PubMed Web of Science ®Google Scholar
• •The time-course of MAC deposition is followed over varying periods of ischaemia and reperfusion. It is shown that reperfusion greatly accelerates MAC accumulation.
   Google Scholar
• ITO W, SCHAFER HJ, BHAKDI S et al: Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rabbits. Cardiovasc. Res. (1996) 32(2)294–305.
   Google Scholar
• KILOGRE KS, PARK JL, TANHEHCO EJ, BOOTH EA, MARKS RM, LUCCHESI BR: Attenuation of interleukin-8 expres-sion in C6-deficient rabbits after myocardial ischemia/reperfusion. j Mol. Cell. Cardiol. (1998) 30(1)75–85.
   Google Scholar
• MAROKO PR, CARPENTER CB, CHIARIELLO M et al.: Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion. J. Clin. Invest. (1978) 61 (3):661–670.
   PubMed Web of Science ®Google Scholar
• BUERKE M, MUROHARA T, LEFER AM: Cardioprotectiveeffects of a Cl esterase inhibitor in myocardial ischemia and reperfusion. Circulation (1995) 91(2)393–402.
   Google Scholar
• •The efficacy of treatment with C1-esterase inhibitor demonstrates that the classical pathway of complement significantly contributes to reperfusion injury.
   Google Scholar
• BLACK SC, GRALINSKI MR, FRIEDRICHS GS, KILGORE KS, DRISCOLL EM, LUCCHESI BR: Cardioprotective effects of heparin or N-acetylheparin in an in vivo model of myocardial ischaemic and reperfusion injury. Cardio-vasc. Res. (1995) 29(5):629–636.
   PubMed Web of Science ®Google Scholar
• GRALINSKI MR, DRISCOLL EM, FRIEDRICHS GS, DENARDIS MR, LUCCHESI BR: Reduction of myocardial necrosis after glycosaminoglycan administration: effects of a single intravenous administration of heparin or N-acetlyheparin 2 hours before regional ischemia and reperfusion. J. Cardiovasc. Pharmacol. Ther. (1996) 1(3):219–228.
   PubMedGoogle Scholar
• PARK JL, KILGORE KS, KEITH KB, BOOTH EA, MURPHY KL, LUCCHESI BR: N-acetylheparin pretreatment reduces infarct size in the rabbit. Pharmacology (1999) 58(3):120–131.
   PubMed Web of Science ®Google Scholar
• TANHEHCO EJ, KILGORE KS, NAYLOR KB, PARK JL, BOOTH EA, LUCCHESI BR: Reduction of myocardial infarct size after ischemia and reperfusion by the glycosaminoglycan pentosan polysulfate. J. Cardio-vasc. Pharmacol. (1999) 34(1):153–161.
   PubMed Web of Science ®Google Scholar
• BUERKE M, PRUFER D, DAHM M, OELERT H, MEYER J, DARIUS H: Blocking of classical complement pathway inhibits endothelial adhesion molecule expression and preserves ischemic myocardium from reperfu-sion injury. J. Pharmacol Exp. Therapeut. (1998) 286(1)429–438.
   Google Scholar
• •This study demonstrates the importance of complement in initiating deleterious cellular responses during reperfusion aside from cell lysis.
   Google Scholar
• SHINGU M, NONAKA S, NISHIMUKAI H, NOBUNAGA M, KITAMURA H, TOMO-OKA K: Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils. Clin. Exp. Immunol (1992) 90(1)72–78.
   Google Scholar
• TANHEHCO EJ, YASOJIMA K, MCGEER PL, LUCCHESI BR: Acute cocaine exposure upregulates complement expression in the rabbit heart. J. Pharmacol. Exp. Ther. (2000) 292(1):201–208.
   PubMed Web of Science ®Google Scholar
• TANHEHCO EJ, YASOJIMA K, MCGEER PL, WASHINGTONRA, LUCCHESI BR: Free radicals upregulate comple-ment expression in the rabbit isolated heart. Am. J. Physiol. (In press).
   Google Scholar
• ROSSEN RD, MICHAEL LH, HAWKINS HK et al.: Cardiolipin-protein complexes and initiation of complement activation after coronary artery occlusion. Circ. Res. (1994) 75(3):546–555.
   PubMed Web of Science ®Google Scholar
• KAPLAN MH, VOLANAKIS JE: Interactions of C-reactive protein with the complement system: I. consumption of human complement associated with the reaction of C-reactive protein with pneumococcal polysaccharide and with the choline phosphatides, lectin and sphingomyelin. j Immunol. (1974) 112(6)2135–2147.
   Google Scholar
• MOLD C, GEWURZ H: Inhibitory effects of C-reactive protein on alternative C pathway activation by liposomes and Streptococcus pneumoniae. J. Immunol (1981) 127(5):2089–2092.
   PubMed Web of Science ®Google Scholar
• MOLD C, KINGZETTE M, GEWURZ H: C-reactive protein inhibits pneumococcal activation of the alternative pathway by increasing the interaction between factor H and C3b. J. Immunol (1984) 133(2):882–885.
   PubMed Web of Science ®Google Scholar
• LAGRAND WK, NIESSEN HW, WOLBINK G-J et al.: C-reactive protein colocalizes with complement in human hearts during acute myocardial infarction. Circulation (1997) 95 (1) :97–103.
   PubMed Web of Science ®Google Scholar
• SECCOMBE JF, SCHAFF HV: Coronary artery endothelialfunction after myocardial ischemia and reperfusion. Ann. Thorac. Surg. (1995) 60(3):778–788.
   PubMed Web of Science ®Google Scholar
• HINDMARSH EJ, MARKS RM: Complement activation occurs on subendothelial extracellular matrix in vitro and is initiated by retraction or removal of overlying endothelial cells. J. Immunol. (1998) 160 (12) :6128–6136.
   PubMed Web of Science ®Google Scholar
• STAHL GL, REENSTRA WR, FRENDL G: Complement-mediated loss of endothelium-dependent relaxation of porcine coronary arteries: role of the terminal membrane attack complex. Circ. Res. (19 9 5) 76(4)575–583.
   Google Scholar
• DAVIES MJ, BLAND MJ, HARTGARTNER WR, ANGELINI A,THOMAS AC: Factors influencing the presence or absence of acute coronary thrombi in sudden ischemic death. Eur. Heart 1 (1989) 10(3)203–208.
   Google Scholar
• FUSTER V: LEWIS A CONNER MEMORIAL LECTURE. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation (1994) 90(0:2126–2146.
   Google Scholar
• VAN DER WAL AC, BECKER AE, VAN DER LOOS CM, DAS PK: Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation (1994) 89(1)36–44.
   Google Scholar
• RINDER CS, RINDER HM, SMITH MJ et al.: Selective blockade of membrane attack complex formation during simulated extracorpeal circulation inhibits platelet but not leukocyte activation. J. Thoracic Cardio-vasc. Surg. (1999) 118(3):460–466.
   PubMed Web of Science ®Google Scholar
• RINDER CS, RINDER HM, JOHNSON K et al.: Role of C3cleavage in monocyte activation during extracorpeal circulation. Circulation (1999) 100(5)553–558.
   Google Scholar
• WAUTIER JL, OLLIER-HARTMANN MP, KADEVA H, COHEN F, HARTMANN L, CAEN JP: First component of complement and thrombosis. Thromb. Haemost. (1981) 45 (3):247–251.
   PubMed Web of Science ®Google Scholar
• PEERSCHKE El, REID KB, GHEBREHIWET B: Platelet activation by Clq results in the induction of alphaIlb/beta3 integrins (GpIlb-III0 and the expres-sion of P-selectin and procoagulant activity. J. Exp. Med. (1993) 178(2):579–587.
   PubMed Web of Science ®Google Scholar
• •The classical pathway component, Clq, activates platelets, which compose the bulk of thrombii.
   Google Scholar
• OZADA C, LEVIN RI, HUIE M et al.: Identification of Clq as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular adhesion molecule 1. Proc. Nag Acad. Sci. USA (1995) 92(18):8378–8382.
   PubMed Web of Science ®Google Scholar
• HOLLANDER W, COLOMBO MA, KIRKPATRICK B, PADDOCK J: Soluble proteins in the human atheroscle-rotic plaque. With special reference to immunoglobu-lins, C3-complement component, a-antitrypsin and a2-macroglobulin. Atherosclerosis (1979) 34(4)391–405.
   Google Scholar
• HANSSON GK, HOLM J, KRAL IG: Accumulation of IgGand complement factor C3 in human arterial endothe-lium and atherosclerotic lesions. Acta. Pathol. Microbiol. Immunol. Scand. (1984) 92(6):429–435.
   Google Scholar
• VLAICU R, RUS HG, NICULESCU F, CRISTEA A: Immuno-globulins and complement components in human aortic atherosclerotic intima. Atherosclerosis (1985) 55(1)35–50.
   Google Scholar
• SCHMEIDT W, KINSCHERF R, DEIGNER HP et al.: Comple-ment C6 deficiency protects against diet-induced atherosclerosis in rabbits. Arterioscler. Thromb. Vasc. Biol. (1998) 18(10:1790–1795.
   PubMed Web of Science ®Google Scholar
• PANG AS, MINTA JO: Inhibition of vitamin D2-inducedarteriosclerosis in rats by depletion of complement with cobra venom factor. Artery (1980) 7(2):109–122.
   PubMedGoogle Scholar
• FRANGI D, GARDINALI M, CONCIATO L, CAFARO C, POZZONI L, AGOSTONI A: Abrupt complement activa-tion and transient neutropenia in patients with acute myocardial infarction treated with streptokinase. Circulation (1994) 89 (0 :76–80.
   PubMed Web of Science ®Google Scholar
• AGOSTONI A, GARDINALI M, FRAGI D: Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction: a comparison between streptokinase and recombinant tissue-type plasminogen activator. Circulation (1994) 90(6)2666–2670.
   Google Scholar
• KOWALSKI J, KOSMIDER M, PAWLICKI L et al.: Comple-ment activates neutrophils during PCTA procedure in patients with unstable angina pectoris. Int. J. Cardiol. (1997) 58(3):229–240.
   PubMed Web of Science ®Google Scholar
• SAWADA M, YANAMOTO H, NAGATA I et al. Prevention of neointimal formation by a serine protease inhibitor, FUT-175, after carotid balloon injury in rats. Stroke (1999) 30(3):644–650.
   PubMed Web of Science ®Google Scholar
• AGOSTONI A, GARDINALI M, FRANGI D et al.: Activationof complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombi-nant tissue-type plasminogen activator. Circulation (1994) 90(6)2666–2670.
   Google Scholar
• VAN OEVEREN W, KAZATCHKINE MD, DESCAMPS-LATSCHA B: Deleterious effects of cardiopulmonary bypass. A prospective study of bubble versus membrane oxygenation. J. Thorac. Cardiovasc. Surg. (1985) 89(6)888–899.
   Google Scholar
• WESTABY S: Organ dysfunction after cardiopulmonarybypass. A systemic inflammatory reaction initiated by extracorpeal circuit. Intensive Care Med. (1987) 13 (2):89–95.
   PubMed Web of Science ®Google Scholar
• GILLINOV AM, DEVALERIA PA, WINKELSTEIN JA et al.: Complement inhibition with soluble complement receptor Type 1 in cardiopulmonary bypass. Ann. Thorac. Surg. (1993) 55(3):619–624.
   PubMed Web of Science ®Google Scholar
• CHEN JC, HUYNH TN, SERNA DL et al.: Alternativepathway of complement is activated during in vitro ventricular assist. J. Invest. Med. (1999) 47(9):502–506.
   PubMed Web of Science ®Google Scholar
• KROHN CD, REIKERÃS, MOLINES TE: Complement activation and increased systemic and pulmonary vascular resistance indices during infusion of postop-eratively drained untreated blood. Br. J. Anaesth. (1999) 82 (1):47–51.
   PubMed Web of Science ®Google Scholar
• BALDWIN WM, SAMANIEGO-PICOTA M, KASPER EK et al. Complement deposition in early cardiac transplant biopsies is associated with ischemic injury and subsequent rejection episodes. Transplantation (1999) 68(6)894–900.
   Google Scholar
• GEERLING RA, ANSARI AA, LAFOND-WALKER AM, BAUMGARTNER WA, HERSKOWITZ A: Accelerated arteriosclerosis in aortic grafts: a role for activated complement and IgM antibody in early lesion develop-ment. Trans. Proc. (1998) 30(4):1017–1019.
   PubMed Web of Science ®Google Scholar
• VAKENTA A, LAURILA P, MERI S: Loss of expression of protectin (CD59) is associated with complement membrane attack complex deposition in myocardial function. Lab. Invest. (1992) 67(5):608–615.
   PubMed Web of Science ®Google Scholar
• VAKENTA A, LAURILA P, MERI S: Regulation of comple-ment membrane attack complex formation in myocar-dial infarction. Am. J. Pathol. (1993) 143(1):65–75.
   PubMed Web of Science ®Google Scholar
• VAKENTA A, LAURILA P, MERI S: Co-deposition of clusterin with the complement membrane attack complex in myocardial infarction. Immunology. (1993) 80 (2) :177–182.
   PubMed Web of Science ®Google Scholar
• VAKENTA A, MORGAN BP, TIKKANEN I, HELIN K, LAURILA P, MERI S: Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium. Am. J. Pathol. (1994) 144(6):1357–1369.
   PubMed Web of Science ®Google Scholar
• VAKEVA A, MERI S: Complement activation and regulator expression after anoxic injury of human endothelial cells. APMIS (1998) 106 (12) :1149–1156.
   PubMed Web of Science ®Google Scholar
• WEISMAN HA, BARTOW T, LEPPO MK et al: Soluble human complement receptor Type 1: in vivo inhibitor of complement suppressing post-ischemic myocar-dial inflammation and necrosis. Science (1990) 249(4965):146–151.
   PubMed Web of Science ®Google Scholar
• ••The first study to demonstrate the efficacy of sCR1 to amelio-rate myocardial reperfusion injury in vivo.
   Google Scholar
• SHANDELYA SML, KUPPUSAMY P, HERSKOWITZ A, WEISFELDT ML, ZWEIER JL: Soluble complement receptor Type 1 inhibits the complement pathway and prevents contractile failure in the postischemic heart: evidence that complement activation is required for neutrophil-mediated reperfusion injury. Circulation (1993) 88 (6) 2812–2826.
   PubMed Web of Science ®Google Scholar
• PRUITT SK, BALDWIN WM 3rd, MARSH HC, Jr., LIN SS, YEH CG, BOLLINGER RR: The effect of soluble complement receptor Type 1 on hyperacute xenograft rejection. Transplantation (1991) 52(5) :868–873.
   Google Scholar
• HILL J, LINDSAY TF, ORITZ F, YEH CG, HECHTMAN HB, MOORE FD, Jr.: Soluble complement receptor Type 1 ameliorates the local and remote organ injury after intestinal ischemia-reperfusion in the rat. J. Immunol. (1992) 149(5):1723–1728.
   Google Scholar
• PRUITT SK, BOLLINGER RR, COLLINS BH et al.: Effect of continuous complement inhibition using soluble complement receptor Type 1 on survival of pig-to-primate cardiac xenografts. Transplantation (1997) 63(6)900–902.
   Google Scholar
• GOODFELLOW RM, WILLIAMS AS, LEVIN JL, WILLIAMS BD, MORGAN BP: Local therapy with soluble comple-ment receptor 1 (sCR1) suppresses inflammation in rat mono-articular arthritis. Clin. Exp. Immunol. (1997) 110 (1):45–52.
   PubMed Web of Science ®Google Scholar
• HOMEISTER JW, SATOH PS, KILGORE KS, LUCCHESI BR: Soluble complement receptor Type 1 prevents human complement-mediated damage of the rabbit isolated heart. J. Immunol. (1993) 150(3):1055–1064.
   PubMed Web of Science ®Google Scholar
• MEDOF ME, NUSSENZWEIG V: Control of the function of substrate-bound C4b-C3b by the complement receptor Crl. J. Exp. Med. (1984) 159(6):1669–1685.
   PubMed Web of Science ®Google Scholar
• IIDA K, NUSSENZWEIG V: Complement receptor is an inhibitor of the complement cascade. J. Exp. Med. (1981) 153 (5):1138–1150.
   PubMed Web of Science ®Google Scholar
• MEDOF ME, IIDA K, MOLD C, NUSSENZWEIG V: Unique role of the complement receptor CR1 in the degrada-tion of C3b associated with immune complexes. J. Exp. Med. (1982) 156(6):1739–1754.
   PubMed Web of Science ®Google Scholar
• SCESNEY SM, MAKRIDES SC, GOSSELIN PL eta].: A soluble deletion mutant of the human complement receptor Type 1, which lacks the C4b binding site, is a selective inhibitor of the alternative complement pathway. Eur. Immunol (1996) 26(8):1729–1735.
   Google Scholar
• GRALINSKI MR, WIATER BC, ASSENMACHER AN, LUCCHESI BR: Selective inhibition of the alternative complement pathway by sCR1 (des LHR-A] protects the rabbit isolated heart from human complement-mediated damage. Immunopharm. (1996) 34(2-3):79–88.
   PubMed Web of Science ®Google Scholar
• RITTERSHAUS CW, THOMAS LJ, MILLER DP: Recombi-nant glycoproteins that inhibit complement activation and also bind the selectin adhesion molecules. J. Biol. Chem. (1999) 274(16):11237–11244.
   PubMed Web of Science ®Google Scholar
• •This investigation characterises a promising new comple-ment inhibitor which also blocks leukocyte accumulation.
   Google Scholar
• ZACHAROWSKI K, OTTO M, HAFNER G, MARSH HC, THIEMERMANN C: Reduction of myocardial infarct size with sCR1sLex, an alternatively glycosylated form of human soluble complement receptor Type 1 (sCR1), possessing sialyl Lewis x. Br. J. Pharmacol. (1999) 128(5)945–952.
   Google Scholar
• •When tested in a model of ischaemia/reperfusion, sCR1sLex proved effective in reducing reperfusion injury, setting this molecule as a potential therapeutic agent.
   Google Scholar
• HUANG J, KIM LJ, MEALEY R eta].: Neuronal protection in stroke by an sLex-glycosylated complement inhibi-tory protein. Science (1999) 285(5427):595–599.
   Google Scholar
• MULLIGAN MS, WARNER RL, RITTERHAUS CW et al.: Endothelial targeting and enhanced antiinflammatory effects of complement inhibitors possessing sialyl Lewis x moieties. J Immunol. (1999) 162(8):4952–4959.
   PubMed Web of Science ®Google Scholar
• HORSTICK G, HEIMANN A, GOTZE 0 et al.: Intracoro-nary application of Cl esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and reperfusion. Circ. Res. (1997) 95(3):701–708.
   Google Scholar
• BAUERNSCHMITT R, BOHRER H, HAGL S: Rescue therapy with Cl-esterase inhibitor concentrate after emergency coronary surgery for failed PCTA. Intensive Care Med. (1998) 24(6):635–638.
   PubMed Web of Science ®Google Scholar
• HIGGINS PJ, KO J-L, LOBELL R, SARDONINI C, ALESSI MK, YEH CG A soluble chimeric complement inhibitory protein that possesses both decay-accelerating and Factor I cofactor activities. J. Immunol. (1997) 158(6) 2872–2881
   PubMed Web of Science ®Google Scholar
• FINCH AM, WONG AK, PACZKOWSKI NJ et al.: Low-molecular-weight peptidic and cyclic antagonists of the receptor for the complement factor C5a. J. Med. Chem. (1999) 42(10:1965–1974.
   PubMed Web of Science ®Google Scholar
• TSUJI RF, MAGAE J, NAGAI K, YAMASAKI M: Effects of L-156, 602, a C5a receptor antagonist, on mouse experimental models of inflammation. Biosci. Biotech. Biochem. (1992) 56(12)2034–2036.
   Google Scholar
• HELLER T, HENNECKE M, BAUMANN U et al.: Selection of a C5a receptor antagonist from phage libraries attenu-ating the inflammatory response in immune complex disease and ischemia/reperfusion injury. J. Immunol (1999) 163(2): 985–994.
   PubMed Web of Science ®Google Scholar
• VAKEVA AP, AGAH A, ROLLINS SA, MATIS LA, LI L, STAHL GL: Myocardial infarction and apoptosis after myocar-dial ischemia and reperfusion: role of the terminal complement components and inhibition by anti-05 therapy. Circulation (1998) 97(22)2259–2267.
   Google Scholar
• •Targeting C5 prevents the formation of C5a and the MAC while allowing the production of the opsonins C3a and C4a.
   Google Scholar
• DWYER JM: Manipulating the immune system with immunoglobulins. N EngI.J Med. (1992) 326 (2):107–116.
   PubMed Web of Science ®Google Scholar
• KAVERI SV, DIETRICH G, HUREZ V, KAZATCHKINE MD: Intravenous immunoglobulins (WI& in the treatment of autoimmune diseases. Clin. Exp. Immunol. (1991) 86(2):192–198.
   PubMed Web of Science ®Google Scholar
• BASTA M, LANGLOIS PF, MARQUES M, FRANK MM, FRIES LF: High-dose intravenous immunoglobulin modifies complement-mediated in vivo clearance. Blood (1989) 74(1)326–333.
   Google Scholar
• MILETIC VD, HESTER CG, FRANK MM: Regulation of complement activity by immunoglobulin: I. Effect of immunoglobulin isotype on C4 uptake on antibody-sensitized sheep erythrocytes and solid phase immune complexes. J. Immunol. (1996) 156(2):749–757.
   Google Scholar
• NICOLETTI A, KAVERI S, CALIGIURI G, BARIETY J, HANSSON GK: Immunoglobulin treatment reduces atherosclerosis in apo E knockout mice. J. Clin. Invest. (1998) 102(5):910–918.
   PubMed Web of Science ®Google Scholar
• ECKER EE, GROSS P: Anticomplementary power of heparin. J. Infect. Dis. (1929) 44:250–253.
   Google Scholar
• SAHU A, PANGBURN MK: Identification of multiple sites of interaction between heparin and the complement system. Mol. Immunol (1993) 30(7):679–684.
   PubMed Web of Science ®Google Scholar
• CALDWELL EEO, ANDREASEN AM, BLIETZ MA et al.: Heparin binding and augmentation of Cl inhibitor activity. Arch. Biochem. Biophys. (1999) 361(2):215–222.
   PubMed Web of Science ®Google Scholar
• BOACKLE RJ, CAUGHMAN GB, VESELY J, MEDGYESI, FUDENBERG HH: Potentiation of factor H by heparin: a rate-limiting mechanism for inhibition of the alterna-tive complement pathway. Ma Immunol. (1983) 20(10:1167–1164.
   Google Scholar
• WEILER JM, LINHARDT RJ: Comparison of the activity of polyanions and polycations on the classical and alternative pathways of complement. Immunopharm. (1989) 17(2):65–72.
   PubMed Web of Science ®Google Scholar
• MUROHARA T, GUO J, DELYANI JA, LEFER AM: Cardio-protective effects of selective inhibition of the two complement activation pathways in myocardial ischemia and reperfusion injury. Meth. Find. Exp. Clin. Pharmacol. (1995) 17(8):499–507.
   PubMed Web of Science ®Google Scholar
• FRIEDRICHS GS, KILGORE KS, MANLEY PJ, GRALINSKI MR, LUCCHESI BR: Effects of heparin and N-acetyl heparin on ischemia/reperfusion-induced alterations in the rabbit isolated heart. Circ. Res. (1994) 75(0701–710.
   PubMed Web of Science ®Google Scholar
• •Heparin's complement-inhibiting effect may be one mechanism by which this glycosaminoglycan protects the ischaemic isolated heart.
   Google Scholar
• MAFFRAND JP, HERGERT JM, BERNAT A et al.: Experi-mental and clinical pharmacology of pentosan polysulfate. Semin. Thromb. Hemost. (1991) 17 (Suppl. 2):186–198.
   Google Scholar
• KILGORE KS, NAYLOR KB, TANHEHCO EJ, PARK JL, BOOTH EA, LUCCHESI BR: The semi-synthetic polysac-charide pentosan polysulfate prevents complement -mediated injury in the rabbit perfused heart. J. Pharmacol. Exp. Ther. (1998) 285(3):987–994.
   PubMed Web of Science ®Google Scholar
• SMITH MM, GHOSH P, NUMATA Y, BANSAL MK: The effects of orally administered calcium pentosan polysulfate on inflammation and cartilage degrada-tion produced by rabbit joints by intraarticular injection of a hyaluronate-polylysine complex. Arthritis Rheum. (1994) 37(1):125–136.
   PubMed Web of Science ®Google Scholar
• HANNO PM: Analysis of long-term Elmiron therapy for interstitial cystitis. Urology (1997) 49 (Suppl. 5A):93–99.
   Google Scholar
• THOMAS H, MAILLET F, LETOURNEUR D, JOZEFONVICZ J, FISCHER E, KAZATCHKINE MD: Sulfonated dextran inhibits complement activation and complement-dependent cytotoxicity in an in vitro model of hyperacute xenograft rejection. Mol Immunol (1996) 33 (7-8):643–648.
   PubMed Web of Science ®Google Scholar
• WUILLEMIN WA, DE VELTHUIS, LUBBERS YT, DE RUIG CP, ELDERING E, HACK CE: Potentiation of Cl inhibitor by glycosaminoglycans: dextran sulfate species are effective inhibitors of in vitro complement activation in plasma. J. Immunol. (1997) 159(01953–1960.
   PubMed Web of Science ®Google Scholar
• KRUMDIECK R, HOOK M, ROSENBERG LC, VOLANAKIS JE: The proteoglycan decorin binds Clq and inhibits the activity of the Cl complex. J. Immunol. (1992) 149(103695–701.
   Web of Science ®Google Scholar
• GRALINSKI MR, PARK JL, OZECK MA, WIATER BC, LUCCHESI BR: LU 51198, a highly sulfated, low -molecular-weight heparin derivative, prevents complement-mediated myocardial injury in the perfused rabbit heart. J. Pharmacol. Exp. Ther. (1997) 282(2)554–560.
   Google Scholar
• KILOGRE KS, HOMEISTER JW, SATOH PS, LUCCHESI BR: Sulfhydryl compounds, captopril and MPG inhibit complement-mediated myocardial injury. Am. J. Physiol. (1994) 266:H28-H35 (Heart Circ. Physiol. 35).
   Google Scholar
• FUSE I, HIGUCHI W, TOBA K, AIZAWA Y: Inhibitory mechanism of human platelet aggregation by nafamo-stat mesilate. Platelets (1999) 10(4):212–218.
   PubMed Web of Science ®Google Scholar
• SUGITA H, ISHIKO T, IKEI S, HIROTA M, OGAWA M: FUT-175 inhibits the production of IL-6 and IL-8 in human monocytes. Res. Commun. Mol. Path. Pharmacol (1999) 103(1):57–64.
   PubMed Web of Science ®Google Scholar
• SAWA Y, ICHIKAWA H, KAGISAKI K, OHATA T, MATSUDA H: Interleukin-6 derived from hypoxic myocytes promotes neutrophil-mediated reperfusion injury in myocardium. J. Thorac. Cardiovasc. Surg. (1998) 116(3):511–517.
   PubMed Web of Science ®Google Scholar
• TANAKA K, KONDO C, TAKAGI K et al.: Effects of nafamostat mesilate on platelets and coagulofibri-nolysis during cardiopulmonary bypass surgery. ASAIO J (1993) 39(3):M545–M549.
   PubMedGoogle Scholar
• MELLGREN K, SKOGBY M, FRIBERG LG, TENGBORN L, WADENVIK H: The influence of a serine protease inhibitor, nafamostat mesilate, on plasma coagulation and platelet activation during experimental Extracor-peal Life Support (ECLS). Thromb. Haemost. (1998) 79(2)342–347.
   Google Scholar
• AOYAMA T, INO Y, OZEKI M et al. Pharmacological studies of FUT-175, nafamstat mesilate. I. inhibition of protease activity in in vitro and in vivo experiments. Jpn. j Pharmacol. (1984) 35(3):203–227.
   Google Scholar
• KARI N, SAKAI Y, HITOMI Y, FUJII M: New synthetic inhibitor of the alternative complement pathway. Immunology (1983) 49(4):685–691.
   PubMed Web of Science ®Google Scholar
• INAKI R, MIYATA T, MAEDA K, SUGIYAMA S, MIYAMA A, NAKASHIMA I: FUT-175 as a potent inhibitor of C5/C3 convertase activity for production of C5a and C3a. Immunol. Lett. 27(1):49–52.
   Google Scholar
• ISSEKUTZ AC, ROLAND DM, PATRICK RA: The effect of FUT-175 (nafamstat mesilate) on C3a, C4a and C5a generation in vitro and inflammatory reactions in vivo. Int. J. Immunopharm. (1990) 12(1):1–9.
   PubMed Web of Science ®Google Scholar
• SAHU A, KAY BK, LAMBRIS JD Inhibition of human complement by C3-binding peptide isolated from a phage-displayed random peptide library. J. Immunol. (1996) 157(2):884–891.
   PubMed Web of Science ®Google Scholar
• NILSSON B, LARSSON R, HONG J et al. Compstatin inhibits complement and cellular activation in whole blood in two models of extracorpeal circulation. Blood (1998) 92(5):1661–1667.
   PubMed Web of Science ®Google Scholar
• FIANE AE, MOLLNES TE, VIDEM V et al. Compstatin, a peptide inhibitor of C3, prolongs survival of ex vivo perfused pig xenografts. Transplantation (1999) 6(1) 52–65
   Google Scholar
• MURRY CE, JENNINGS RB, REIMER KA: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation (1986) 74(5):1124–1136.
   PubMed Web of Science ®Google Scholar
• TANHEHCO EJ, YASOJIMA K, McGEER PL et al. Preconditioning reduces tissue complement gene expression in the rabbit isolated heart. Am. J. Physiol. (1999) 277:2373-2380 (Heart Circ. Physiol. 46).
   Google Scholar
• •Reduction of local complement expression may be one mechanism by which preconditioning exerts its cardiopro-tective effects.
   Google Scholar
• TANHEHCO EJ, YASOJIMA K, MCGEER PL, MCGEER EG, LUCCHESI BR: Preconditioning reduces complement gene expression in vivo. Am. J. Physiol. (In press).
   Google Scholar
• GROSS GJ, AUCHAMPACH JA: Blockade of ATP-sensitive potassium channels prevents myocardial precondi-tioning in dogs. Circ. Res. (1992) 70(2):223–233.
   PubMed Web of Science ®Google Scholar
• GROSS GJ: ATP-sensitive potassium channels and myocardial preconditioning. Basic Res. Cardiol (1995) 90(3)85–88.
   Google Scholar
• GARLID KD, PAUCEK P, YAROV-YAROVOY V et al.: Cardioprotective effect of diazoxide and its interaction with mitochondrial ATP-sensitive K channels: possible mechanism of cardioprotection. Circ. Res. (1997) 81(6):1072–1082.
   PubMed Web of Science ®Google Scholar
• GROVER GJ, MCCULLOUGH JR, HENRY DE, CONDER ML, SLEPH PC: Anti-ischemic effects of the potassium channel activators pinacidil and cromakalim and the reversal of these effects with the potassium channel blocker glyburide. J. Pharmacol. Exp. Ther. (1989) 251(0:98–104.
   PubMed Web of Science ®Google Scholar