Basic Research in Cardiology Basic Res Cardio188:150-154 (1993) lnterleukin-8 is not involved in the increased chemotactic activity of peripheral blood plasma during acute myocardial infarction T. Siminiak 1, J.-M. Schr6der 2, M. Sticherling2, and H. Wysocki 2 t Department Intensive Therapy, Academy of Medicine, Poznan, Poland 2 Department of Dermatology, University of Kiel, FRG Summary: Polymorphonuclear neutrophils (PMN) are known to participate in the development of tissue injury during myocardial infarction due to both free oxygen radicals release, as well as to their involvement in the "no-reflow" phenomenon. We have previously shown that pheripheral blood plasma (obtained from patients with acute myocardial infarction) has chemotactic activity for PMN and is able to induce PMN adherence as well as superoxide anion production. To investigate whether intcrleukin-8 (IL-8/NAP-1), a potent chemotactic factor for PMN, is involved in plasma-mediated PMN stimulation, we measured plasma levels of IL-8 in five patients with transmuraI myocardial infarction with highly sensitive enzyme-linked immunosorbent assay (ELISA) using specific antibodies. Blood samples were taken immediately after patients' admission, within 15 and 30 rain of treatment with intravenous nitrates, as well as after 1, 2, 3, and 7 days. All samples expressed IL-8 activity within the detection limit (0.4 ng/ml) as observed at the basal state. Thus, IL-8 may not be considered as responsible for the chcmotactic acitivity in peripheral blood in patients with myocardial infarction. Key words: Polymorphonuclear neutrophils - acute myocardial infarction - interleukin-8 - chemotac- tic activity Introduction Participation of polymorphonuclear neutrophils (PMN) in the development of tissue injury during acute myocardial infarction is well documented. Activated PMN aggregate and adhere to endothelium (6) that leads to subsequent leukoembolization of coronary capil- laries and impairment of blood flow. Furthermore, activated PMN release large amounts of free oxygen radicals and proteolytic enzymes (8, 15) that exert a direct cytotoxic effect on myocytes. Increased PMN migration to ischemic myocardium in response to locally released chemotactic stimuli was shown in several experimental studies to enhance the extent of irreversibly injured myocardium. We have previously reported that peripheral blood plasma from patients with myocardial infarction has chemotactic activity for PMN obtained from healthy donors and is able to augment PMN adherence (9, 10), as well as inducing PMN superoxide anion production (26). Systemic activation of PMN as a result of myocardial infarction was shown by evaluation of PMN aggregation in peripheral blood (1, 25). The purpose of the present study was to verify if interleukin-8, a potent chemotactic factor for PMN, is involved in increased chemotactic activity of peripheral blood plasma during AMI. 777