[Process of platelets activation by streptokinase].

This study concerns the influence of streptokinase and antistreptokinase antibodies on rabbits platelets in blood plasma depleted of plasminogen. The immune complex streptokinase-antibody causes platelets activation, whereas other investigated immune complexes didnot express such activity. Platelets aggregation wasnot detected in any case. It was determined that streptokinase induces platelets activation in the rabbit plasma with high titre of antistreptokinase antibodies in absence of plasminogen.

[Process of complexation of prothrombine and fibrin E-fragment].

The study is devoted to research of the blood coagulation key proenzyme complexation process. It is prothrombin, and the E-fragment of fibrin can be a component in blood circulation. It is shown, that non-enzyme activation of prothrombin by the E-fragment proceeds as a result of formation of stable non-covalent prothrombin-E fragment complex. The cringle structures of prothrombin and the N-terminal site of beta-chain of E-fragment of fibrin are important for formation of the given complex. It has been defined, that other fragments of fibrin (D and DD) are not capable to induce amydolytic activity of prothrombin.

[Effect of streptokinase on the content of plasminogen activator inhibitor of type 1].

The influence of streptokinase on plasminogen activators inhibitor of type I (PAI-1) was investigated with the use of model systems in vitro and in vivo. It was defined, that intravenous streptokinase injection causes an increase in PAI-1 content in mammals' blood plasma. Experiments in vitro have shown that the increase in PAI-1 concentration takes place as a result of streptokinase action. It occurs due to platelets activation with subsequent PAI-1 secretion from their a-granules. It is established, that PAI-1 is secreted by platelets both in free and in complex forms. The data obtained in the work, allow to assume, that the simultaneous substantial increase in PAI-1 content with platelets activation, as a result of streptokinase influence, can lead to new thrombotic complications risk.

[Effect of streptokinase on the parameters of haemostasis in model systems in vivo]. / Vplyv streptokinasy na parametry systemy hemostazu v model'nykh systemakh in vivo.

The changes of the haemostasis system parameters were studied under treatment by streptokinase (Sk, thrombolytic agent of bacterial origin) with the use of model systems in vivo. We were especially interested in the study of the changing fibrinolytic system parameters such as tissue type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), plasminogen, alpha2-antiplasmin activities. After treatment by Sk the activity and quantity of t-PA were significantly increased while the activity of PAI-1 was decreased. The parameters of haemostasis system evidenced for a disbalance which occurred under treatment by Sk: decrease of fibrinogen levels and appearance of soluble fibrin and accumulation of fibrin degradation products. Thus analysis of the data has displayed besides the well-known Sk function the influence of Sk on the change of fibrinolytic system potential probably due to its effect on the endothelial cells.

[Effect of tissue-type plasminogen activator and its inhibitor in haemostasis system function in norm and pathology]. / Rol' tkanynnoho aktyvatora plazminohenu ta ioho inhibitora u funktsionuvanni systemy hemostazu za normy ta patolohiï.

The paper is dedicated to the study of structure and physiological functions of tissue type plasminogen activator and its inhibitor PAI-1, changes of these parametres in normal and pathology conditions. The interrelation of the coagulation and the fibrinolytic system during the range of pathologies was studied. It was demonstrated that simultaneous analysis of the coagulation and fibrinolytic systems analysis allow to diagnose the thrombotic complications.