Abstract
The fibrinolytic process includes plasminogen cleavage by different types of plasminogen activators leading to plasmin formation. Plasmin degrades fibrin but also cartilage proteoglycan1 and activates latent collagenase2. Besides its role in hemostasis, fibrinolysis may play a role in tissue remodeling and metastasis of tumor cells3,4. The fibrinolytic process is controlled by inhibitors acting either at the plasminogen activation step or by antiplasmins. An alteration in fibrinolysis was first observed following the injection of certain vaccines5. These changes were reproducible with purified lipopolysaccharides (LPS) from the walls of gram-negative bacteria. After experimental endotoxemia there is first an acceleration of fibrinolysis followed by a late depression. Some of the mechanisms underlying these sequential modifications have been recently clarified by the identification of mediators induced by endotoxin and the ability to study the responses of isolated cells.
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© 1987 Plenum Press, New York
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Dosne, AM., Dubor, F., Chedid, L. (1987). Fibrinolysis in Endotoxemia. In: Paubert-Braquet, M., Braquet, P., Demling, B., Fletcher, J.R., Foegh, M. (eds) Lipid Mediators in the Immunology of Shock. NATO ASI Series, vol 139. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0919-2_27
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DOI: https://doi.org/10.1007/978-1-4613-0919-2_27
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