Abstract
Fibrin is a common finding at inflammatory sites. The formation of persistent fibrin deposits is due to a disturbance in the normally very efficient system for degradation of fibrin, the fibrinolytic system (1). The fibrin surface specifically absorbs both plasminogen and plasminogen activators, with formation of plasmin as a result. This plasmin is partially protected from fibrinolysis inhibitors by the fibrin surface and can activate both the complement system and the kinin system. Eventually, the fibrin is degraded, for example by plasmin or leukocyte elastase, during which process small peptides are released. Some of these peptides have vasoactive and other properties which make them candidates as contributory mediators in the inflammatory process (2,3).
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References
Saldeen, T. (1976). The microembolism syndrome. Microvasc. Res., 11, 227–259.
Saldeen, T. (1982). Fibrin-derived peptides and pulmonary injury. Ann. N.Y. Acad Sci., 384, 319–331.
Saldeen, T. (1983). Vasoactive peptides derived from degradation of fibrinogen and fibrin. Ann. N.Y. Acad. Sci., 408, 424–437.
Hogstorp, H. and Saldeen, T. (1982). Synthesis of α2-antiplasmin by rat liver cells. Thromb. Res., 28, 19–23.
Wegener, T., Bagge, L. and Saldeen, T. (1979). Effect of nicotinic acid on the posttraumatic increase in free fatty acids and fibrinolysis inhibition activity in the rat. Upps. J. Med. Sci., 84, 195–201.
MoCostabella, P., Lindquist, O., Kapanci, Y. and Saldeen, T. (1978). Increased vascular permeability in the delayed microembolism syndrome. Experimental and human finding. Microvasc. Res., 15, 275–286.
McGuire, W.W., Spragg, R.G., Cohen, A.B. and Cochrane, C.G. (1982). Studies on the pathogenesis of the adult respiratory distress syndrome. J. Clin. Invest., 69, 543–553.
Belew, M., Gerdin, B., Porath, J. and Saldeen, T. (1978). Isolation of vasoactive peptides from human fibrin and fibrinogen degraded by plasmin. Thromb. Res., 13, 983–994.
Wallin, R., Saldeen, K., Belew, M., Ohlsson, K. and Saldeen, T. (1985). Purification and characteristics of a vasoactive peptide derived from elastase degradation of human fibrin(ogen). In Fibrinogen, Vol. 3, in press.
Wallin, R., Saldeen, K. and Saldeen, T. (1985). Structure-function studies on a vasoactive pentapeptide derived from plasmin degradation of human fibrin(ogen). In Fibrinogen, Vol. 3, in press.
Andersson, R.G.G., Saldeen, K. and Saldeen, T. (1983). A fibrin(ogen) derived pentapeptide induces vasodilation, prostacyclin release and an increase in cyclic AMP. Thromb. Res., 30, 213–218.
Ito, T., Ogawa, K., Enomoto, I., Hashimoto, H., Kai, I. and Satake, T. (1980). Comparison of the effects of PGI2 and PGE1 on coronary and systemic hemo-dynamics and coronary arterial cyclic nucleotide levels in dogs. In Advances in Prostaglandin and Thromboxane Research, Vol. 7, (eds. B. Samuelsson, P.W. Ramwell, and R. Paoletti), Raven Press, New York, pp. 641–646.
Saldeen, T., Ryan, J.W. and Berryer, P. (1981). A peptide derived from fibrin(ogen) inhibits angiotensin converting enzyme and potentiates the effects of bradykinin. Thromb. Res., 23, 465–470.
Eriksson, M., Saldeen, K., Saldeen, T., Strandberg, K. and Wallin, R. (1983). Fibrin-derived vasoactive peptides release histamine. Int. J. Microcirc. Clin. Exp., 2, 337–345.
Busch, C. and Gerdin, B. (1981). Effect of low molecular weight fibrin degradation products on endothelial cells in culture. Thromb. Res., 22, 33–39.
Gerdin, B., Saldeen, T., Roszkowski, W., Szmigielski, S., Stachurska, J. and Kopec, M. (1980). Immunosuppressive effect of vasoactive peptides derived from human fibrinogen. Thromb. Res., 18, 461–468.
Andersson, P., Brange, C. Saldeen, K. and Saldeen, T. (1985). Fibrin(ogen) derived vasoactive peptides release thromboxane, prostacyclin and histamine in isolated, perfused guinea-pig lung, (in preparation).
Kopec, M., Roszkowski, W., Szmigielski, S., Gerdin, B. and Saldeen, T. (1979). Effect of low molecular weight fibrinogen degradation products on lymphocytes, macrophages and kidney cells in cultures. Thromb. Haemostas. 42, 293.
Roszkowski, W., Stachurska, J., Gerdin, B., Saldeen, T. and Kopec, M. (1985). Suppression of cell-mediated immune reactivity by peptides cleaved from fibrinogen, (submitted for publication).
Saldeen, K., Christie, N., Nelson, W.R. and Movat, H.Z. (1985). Effect of a fibrin(ogen)-derived vasoactive peptide on polymorphonuclear leukocyte emigration. Thromb. Res., 37, 85–89.
Williams, T.J. and Peck, M.J. (1977). Role of prostaglandin-mediated vasodilation in inflammation. Nature, 270, 530–532.
Manwaring, D., Thorning, D. and Currieri, P.W. (1978), Mechanisms of acute pulmonary dysfunction induced by fibrinogen degradation product D. Surgery, 84, 45–54.
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Saldeen, T. (1985). The Fibrinolytic System in Inflammation. In: Higgs, G.A., Williams, T.J. (eds) Inflammatory Mediators. Satellite Symposia of the IUPHAR 9th International Congress of Pharmacology. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-07834-9_9
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DOI: https://doi.org/10.1007/978-1-349-07834-9_9
Publisher Name: Palgrave Macmillan, London
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