The fibrinolytic system in man.
The existence of a system in the human body capable of inducing the dissolution of endogenous pathologically formed thrombi was appreciated in ancient times. Considered in detail in this article are the data that have elucidated the physiologic regulation of which plasmin formation is dependent on, the plasma concentration of plasminogen, availability of activators of plasminogen in the plasma and surrounding tissue environment, the concentration of naturally present inhibitors, and the existence of fibrin in the circulation. Important in this rapidly progressive scientific discipline is consideration of the factors which control the synthesis of the components of this proteolytic enzyme system. Recently abundant information has indicated that this plasminogen-plasmin proteolytic enzyme system can be utilized therapeutically. Knowledge of the mechanisms of this system has permitted identification of agents that can be exogenously administered to releave thrombotic obstruction to blood flow in the venous (pulmonary emboli, deep vein thrombosis) and arterial (peripheral and central vessels) circulatory systems. Particularly important is the demonstration that thrombolytic agents can directly attack and alleviate the immediate cause of acute myocardial infarction. As a result of the innovations in the present decade, it is evident that the plasminogen system can be advantageously employed to reverse the pathologic effects of all thrombotic diseases.
D000933:Antifibrinolytic Agents / Q000627:therapeutic use; D000990:Antithrombin III / Q000494:pharmacology; D001157:Arterial Occlusive Diseases / Q000188:drug therapy; D001161:Arteriosclerosis / Q000097:blood; D003174:Complement C1 Inactivator Proteins / Q000494:pharmacology; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D005337:Fibrin / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D005341:Fibrinolysin / Q000494:pharmacology; D005342:Fibrinolysis / Q000187:drug effects; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D007674:Kidney Diseases / Q000097:blood; D008107:Liver Diseases / Q000097:blood; D009203:Myocardial Infarction / Q000188:drug therapy; D009369:Neoplasms / Q000097:blood; D010958:Plasminogen / Q000032:analysis; D011655:Pulmonary Embolism / Q000188:drug therapy; D013924:Thrombophlebitis / Q000097:blood; D000515:alpha 1-Antitrypsin / Q000494:pharmacology; D000979:alpha-2-Antiplasmin / Q000494:pharmacology; D000511:alpha-Macroglobulins / Q000494:pharmacology
D000933:Antifibrinolytic Agents; D003174:Complement C1 Inactivator Proteins; D005343:Fibrinolytic Agents; D000515:alpha 1-Antitrypsin; D000979:alpha-2-Antiplasmin; D000511:alpha-Macroglobulins; D000990:Antithrombin III; D005337:Fibrin; D005340:Fibrinogen; D010958:Plasminogen; D005341:Fibrinolysin