Lytic solution of platelet-rich plasma clots potentiated platelet response to agonists by action on Ca2+ homeostasis.

Effects of thrombolytic agents and lytic solution of platelet-rich plasma (PRP) clots (LSPC) on platelet activation as indicated by platelet aggregation, generation of malondialdehyde (MDA), and the concentration of intracellular free calcium ([Ca2+]i) in rats were investigated. Neither urokinase nor streptokinase in vitro showed adverse effects on platelet function. The solution of PRP clots incubated either alone (as control) or with urokinase or streptokinase 2000 IU.ml-1 at 37 degrees C for 45 min potentiated the increase of platelet aggregation and MDA formation and produced a persistently high level of [Ca2+]i stimulated by thrombin, and platelet aggregation induced by ADP. But LSPC had no effects on the Ca2+ influx or the release of intracellular stored Ca2+, and no significant difference was found in the promotion of platelet response to agonists between the solution of the clots warmed in the presence or absence of thrombolytic agents. In the thrombosis model in rat abdominal aorta, both urokinase and streptokinase (40,000 IU.kg-1) slightly inhibited electrically stimulated thrombosis. In contrast, LSPC (600 microliters.kg-1) considerably enhanced the thrombosis. These findings suggested that the changes of platelet function in ischemic patients receiving thrombolytic therapy may be mediated by the proteolytic products of clots through acting on [Ca2+]i homeostasis after platelet stimulation rather than by the thrombolytic agents per se.