The current study was designed to elucidate mechanisms responsible for alterations of platelet activation and aggregation in patients with an acute myocardial infarction (AMI) treated with streptokinase (SK). Platelet function and membrane structure were examined prior to and one hour after i. v. administration of SK in 26 patients with an AMI. In 10 patients with a myocardial infarction, not undergoing thrombolytic therapy, in vitro platelet membrane glycoproteins (GP) were examined in platelet rich plasma following incubation with SK. ADP, adrenaline, collagen and ristocetin induced platelet aggregation were studied by Born's method, b-thromboglobulin (bTG) and platelet factor 4 (PF4) concentrations in plasma were determined using ELISA, von Willebrand's factor was determined by agglutination, GP Ib and GP IIb/IIIa by indirect immunofluorescence using appropriate monoclonal antibodies, and the platelet membrane structure by electronic paramagnetic resonance using spin labels. The results obtained confirm that in patients with an AMI treated with SK, platelet function is altered: platelet activation is enhanced, which is manifested by an increase in bTG and PF4 concentrations, and at the same time their aggregation is disturbed. In addition, SK was shown to induce structural changes in protein conformation and in the fluidity of platelet membrane lipids which may be responsible for the alterations in platelet aggregation. Additional reasons for platelet aggregation disturbances may be due to the decrease in platelet GB Ib and IIb/IIIa, as well as a considerable drop in the fibrinogen concentration observed following SK therapy.

Keywords: Streptokinase, Platelet Aggregation, betathromboglobulin, platelet factor 4, platelet glycoproteins, platelet membrane structure