Interaction of epinephrine and ADP in regulation of platelet function in chronic cerebral ischemia

Abstract

The purpose is devoted to test of hypothesis that patients with chronic cerebral ischemia (CCI) have decreased secretion of platelet ADP as the reason of platelet aggregation restriction in response to stimulation of adrenaline. Methods. We used platelet-rich plasma which was separated by centrifugation from peripheral blood of 55 patients with a diagnosis of CCI of stage 1—2. Platelets aggregation was studied on aggregometer Chrono — Log (USA). ADP and Epinephrine were used for platelet stimulation at effective concentration (EC50). Modulatory role of ADP subthreshold doses (0.5 mM) in platelet activation was analyzed with its addition to a suspension of platelets stimulated by agonists (EC50). Results. In 35 patients (group 1) with platelet hyperreactivity to ADP (EC50) response of platelets to Epinephrine was heterogeneous: in 17 cases (48.6%) there was high response (50%) and in 18 cases (51.4%) there was low platelet response to Epinephrine. 20 patients (group 2) had hyporesponsiveness of platelets upon stimulation by both agonists. It was established that the low initial response of platelets to Epinephrinе in vitro might be due to reduced secretion of ADP, i.e. limited adaptive response since administration of ADP subthreshold doses enhances adrenoreactivity of platelets. If pathochemical violations underlying the formation of platelet disadaptation are reversible, it is possible to recover the reaction of platelets to Epinephrine. Conclusion. In reducing the functional response of platelets to Epinephrinе key issue is establishing the reversibility of violations of platelets adaptive response of platelets.