Tissue factors of the coagulation and fibrinolysis systems
Issue title: Microcirculation, Interstitium, Lymph, Pathophysiology and Disease. Proceedings of the International Symposium, Villa La Principessa, Lucca, Italy, June 19–20, 1981
Affiliations: Gaubius Institute TNO, Leiden, The Netherlands, Ribe County Hospital at Esbjerg, Universitiy Centre of South Jutland, 6700 Esbjerg, Denmark
Abstract: When tissues in the body are damaged the injured cells release thromboplastin, plasminogen activator and substances enhancing cell migration and proliferation. Thereby are initiated processes of wound healing and tissue repair. Haemostasis and the termination of an exsudative process are secured by an extrinsic coagulation process initiated by tissue thromboplastin, which is supported by the intrinsic coagulation system by an activation of humoral coagulation factors caused by damaged platelets, and resulting in the formation of plasma thromboplastin. The fibrin formed serves as a matrix for the formation of a granulation tissue induced by the growth promoting substances released from the cells causing migration and proliferation of fibroblasts and angioblasts. During this process the fibrin deposit undergoes resolution caused by activation of the fibrinolytic system. Plasminogen is converted to the active enzyme, plasmin, by the released tissue plasminogen activator. This extrinsic activation is supplemented by an intrinsic pathway by which a humoral plasminogen activator is formed in the blood. Excessive deposits of fibrin remain if the local process of fibrinolysis is unable to cope with the amounts of fibrin formed. This may result from a continuous release of thromboplastin at a site of injury or from a low content of plasminogen activator. Differences in repair processes in various tissues results from the differences in content of tissue thromboplastin and plasminogen activator. Tissues low in plasminogen activator are particularly vulnerable to local fibrin deposition, thrombosis and the formation of excessive amounts of reparative connective tissue. This is seen in the liver and in the kidney cortex. Disseminated deposition of fibrin causes the syndromes of disseminated intravascular coagulation or microembolism, which in acute phases may lead to defibrination, extensive fibrinolysis and death from haemorrhage. Termination of the initiating coagulation process by heparin may then revert the situation and paradoxically terminate haemorrhage.
