Plasminogen
Reference values of plasminogen content in blood plasma - 80-120%.
Plasminogen ( profibrinolysin) is an inactive precursor of the enzyme plasmin( fibrinolysin).Determination of plasminogen is crucial for assessing the state of the fibrinolytic system.
The plasmic system includes four main components: plasminogen, plasmin, activators of fibrinolysis proenzymes and its inhibitors. Plasminogen is converted into plasmin under the influence of physiological activators - substances that activate fibrinolysis. They can be plasma, tissue and exogenous( bacterial) origin. Tissue activators are formed in the tissues of the prostate gland, lungs, uterus, placenta, liver, vascular wall. Activators of plasminogen are contained in secretory fluids( they include, in particular, urokinase, produced in the kidneys).Exogenous plasminogen activator of bacterial origin( streptokinase) activates the plasmin gene, forming an active complex with it.
The plasmic system is primarily designed for fibrin lysis, although plasmin can easily destroy fibrinogen, factors V, VIII, and others. A powerful antiplasmin system( a1-antitrypsin, a2-AP, a2-macroglobulin, ATH) protects these proteins from the action of plasmin, focusing its action on fibrin.
. Disorders in the plasmin system. Under the influence of various pathological processes, the state of the plasmin system and the production of its individual components change. As a result of the activation of the plasmin system, hemostasis is disrupted and the hemorrhagic fibro-rhinolytical syndrome often develops. Clinically, it is manifested by severe bleeding due to multiple defects in the hemostatic system. This syndrome can be latent: bleeding is noted in patients only in the postoperative and postpartum periods with tissue damage. Most often, such conditions are revealed in patients with liver lesions as a result of a decrease in the synthesis of antiplasms, in the defeat of organs rich in plasminogen activators, and in operative interventions on them( in operations for prostate cancer,
lung), less often in patients with strengthenedproduction( drug, bacterial, stress, etc.) of plasminogen activators or their increased concentration( Table).This fibrinolysis, caused by the primary activation of the plasmin system as such and does not reflect the body's response to increased fibrin formation, is the primary fibrinolysis. To correct it, antifibrinolytic drugs like antiproteases( aprotinin, e-aminocaproic acid) are prescribed.
In most cases, secondary fibrinolysis is observed due to the activation of the plasmin system in the formation of fibrin in the body. In secondary fibrinolysis, plasmin activity first increases, and then gradually decreases and, finally, completely disappears due to depletion of plasminogen stores. The concentration and activators of plasminogen are often reduced against the background of a reduced or increased amount of antiplasms( Table).On the ability of a number of drugs to convert inactive plasminogen to plasmin, thrombolytic therapy in patients with MI and thromboembolism is based on the administration of plasminogen activators( most often streptokinase preparations).When carrying out thrombolytic therapy, constant monitoring of the level of plasminogen in the blood is necessary.
Table Changes in the system of hemostasis in primary and secondary fibrinolysis
Table Changes in the hemostatic system in primary and secondary fibrinolysis
The most pronounced shifts in the plasmin system are observed in DIC syndrome, when the activation of fibrinolysis is first a protective, sanogennic reaction, and therefore plasmin inhibitors are contraindicated.
It should be borne in mind that plasminogen, as well as all other proteins of the acute phase, increases in infections, injuries, tumors and in recent months of pregnancy.