EVALUATION OF POLYMORPHO NUCLEAR CELLS (PMN) CYTOTOXIC ACTIVITY FROM PATIENTS WITH ACUTE CORONARY SYNDROMES

Abstract

Objective: Reactive oxygen species (ROS)are known as secondary toxic products of oxygen metabolism from mammalian cells and they are generated within the vascular wall by NADPH oxidase and this process can be stimulated by mechanical stress. The aim of this study was to investigate PMN oxygen dependent cytotoxic activity expressed as a liberation of anion superoxide within the extracellular space (marker of oxidative stress),or intracellular production of superoxide (marker of antimicrobial defense oxygen dependent) by stimulated/non-stimulated PMN for CR3 and fMLP-R by cytochrome C reduction test. Evaluation of responsive cells proportion in controls and patients with acute coronary syndromes at stimulation of CR3 and fMLP-R as well as evaluation of responsive degree of cells. Evaluation of respiratory intensity with intracellular production of superoxide anion (NBT test). Design and method: Our study was done on 21 patients aged 45–72 years old with acute myocardial infarction (AMI(6) and Unstable angina pectoris (U.A.P).(15) admitted in Cardiology Clinique of C.C. Iliescu” Cardiovascular Disease Institute. PMN from patients with (AMI) and (UAP)have been isolated from peripherial blood by centrifugation in density gradient and in vitro stimulated at CR3 and fMLP-R with major role in inflammatory process. Results: There is an increase in superoxide anion levels in patients with cardiovascular pathology both in the presence of zymosan and fMLP. The signal transmitted by CR3 and fMLP-R intensifies generation but not liberation of anion superoxide indicating a mobilization of a complex mechanism of destruction of pathogenes without exacerbation of oxydative stress. Leucocytosis found in patients with UAP suggests the existence of anti-inflammatory signals which determines extravasation of PMN population from bone marrow responsive to potential inflammatory stimuli. Conclusions: Patients with UAP posses a non specific immune defense system accompanied by an increase in the basal potential of oxidative stress.