[ROLE α2-ADRENERGIC RECEPTORS IN REGULATION PLATELET REACTIVITY IN THE ELDERLY AT CHRONIC OBSTRUCTIVE PYELONEPHRITIS].

Objective of the research was to determine involvement of platelets and the role of adrenaline in chronic inflammation maintaining and the initiation of acute inflammatory response in elderly patients with chronic obstructive pyelonephritis against this background. The study includes 60 patients with chronic obstructive pyelonephritis (COPN), which are distributed into two groups: basic - 22 elderly patients (age 73±1,5 years) and the comparison group - 38 middle-aged patients (52,5±2,4 years). The study excluded patients who took antiplatelet drugs and non-selective blockers of α adrenergic receptors at least 1 week before the study. Analysis of platelets adrenoreactivity in vitro was carried out at the time of hospitalization before the start of conservative therapy. Platelet-rich plasma was isolated from peripheral blood by centrifuging. ADP and epinephrine were used in the effective (EC50) and sub-threshold (EC10) concentrations to stimulate platelets. The formation of platelet-leukocyte aggregates was reproduced in vitro upon incubation of stimulated platelets (at a concentration of adrenaline EC50) and intact leukocytes isolated from patient peripheral blood. The study of platelet reactivity revealed that in elderly patients acute inflammatory response realization (relapse of COPN) is against optimal functioning of platelets α2 adrenergic receptors. Significant increase in the number of platelet-leukocyte aggregates is possible. Remission of COPN (the presence of chronic inflammation) in the examined patients of various ages was associated with platelet hypoadrenoreactivity. Increased platelet adrenoreactivity during transition from remission to relapse of COPN in the elderly patients is possible if adequate synthesis of ADP in platelets and its secretion from dense granules are preserved. The observed interaction of adrenaline and ADP with stimulated platelet hyporesponsiveness probably ensures adaptive response aimed at acute inflammatory response in COPN.