The neutrophil granulocyte seems to be intimately involved in the destructive processes leading to myocardial damage observed in ischaemic/reperfusion injuries. The process may cause stress to the peripheral circulating neutrophils leading to exhaustion and decreased function. We conducted a study in which the function of peripheral neutrophil granulocytes was measured in 21 patients with an acute myocardial infarction 0-24 and 48-72 h after the onset of symptoms. Ten patients received thrombolytic treatment (streptokinase). Neutrophil function was judged by superoxide generating capacity and chemotactic ability. Compared to healthy controls neutrophil function was found to be preserved in patients with myocardial infarction. Furthermore, streptokinase treatment of the patients did not modulate neutrophil function. In-vitro studies demonstrated that low concentrations of streptokinase (12-300 U.ml-1) or recombinant plasminogen activator (0.12 micrograms.ml(-1)-3.0 micrograms.ml-1) did not influence neutrophil superoxide generation. However, at higher concentrations (100-10,000 U.ml-1 and 10-100 micrograms.ml-1 respectively) both thrombolytics induced a significant increase in phorbol myristate acetate-stimulated superoxide generation. Neither of the thrombolytics influenced neutrophil chemotaxis in vitro. It is concluded that neither myocardial infarction nor streptokinase treatment decrease superoxide generating capacity or chemotactic ability of circulating neutrophils.