COMPARATIVE EFFECTS OF RECOMBINANT STAPHYLOKINASE AND STREPTOKINASE AN PLATELET-AGGREGATION

Recombinant staphylokinase (RSTA) has been shown to offer promise as a thrombolytic agent. In contrast to streptokinase (SK), few studies ha ve been devoted to possible effects of RSTA on platelets. We have comp ared the capacity of RSTA and SK to trigger platelet aggregation and t o modify ADP (2.5 mu M) response in platelet-rich plasma (PRP) of 25 h ealthy subjects. Thus, exposure of PRP to SK (40 to 50 mu g/ml) induce d platelet aggregation in 6 out of 25 subjects. How ever, under the sa me conditions, RSTA failed to induce platelet aggregation in all cases (25 out of 25 subjects). In contrast to RSTA, SK (0.4 to 50 mu g/ml) greatly reduced ADP-induced platelet aggregation in 12 out of 25 subje cts. Preincubation of plasma with SK is associated with a decrease in the fibrinogen concentration. Furthermore, there was a good correlatio n between SK-induced fibrinogenolysis and SK-induced platelet aggregat ion defect (r(2) = 0.9; p = 0.001). No fibrinogenolysis was observed w hen different amounts of RSTA (0.4 to 50 mu g/ml) were incubated in pl asma for one min. However, there was a marked decrease in fibrinogen l evel (about 50%) when the plasma was incubated for five min with a ver y high concentration of RSTA. SK markedly enhanced the platelet respon se to ADP in 13 out of 25 subjects. In PRP of 6 out of 25 subjects, SK induces platelet aggregation and potentiates platelet response to ADP , however in PRP of 7 out of 25 subjects, SK caused only the increase of platelet response to ADP. The monoclonal antibody anti-Fc gamma RII a1, IV-3 (2 mu g/ml), abolished SK-induced platelet aggregation and SK -enhanced ADP-induced platelet aggregation. In all cases (25 out of 25 subjects), RSTA failed to potentiate platelet response to ADP. These findings confirm that RSTA has a lesser fibrinogenolytic ability than SK and suggest its negligeable effect on platelet function.