Mamedaliieva S. The pathogenetic mechanisms of platelets' functional disorders in the progression of chronic cerebral ischemia

The thesis is devoted to solving actual scientific task of pathophysiology - to analyze the mechanisms of platelets' (Pl) dysfunction on the progression of chronic cerebral ischemia (CCI). The analysis of the clinical, instrumental and laboratory data from 80 patients with CCI and 35 patients with ischemic stroke (IS) was carried out at points 24 hours after of standard medication initiation and 8-14 days after hospital treatment. Platelet reactivity was assessed with optic agregometry by measurement of platelet aggregation induced by ADP (5 µM), epinephrine (5µM), platelet aggregation factor (PAF, 150 µM). Severity of Pl individual reactivity with the progression CCI is caused by the presence of different phenotypes of Pl, which differentiate by functional state clusters of a2-adrenergic receptors, purine (R2Y1 and P2Y12) and PAF receptors, as well as the degree of participation of systematic, auto- and paracrine factors in the pathogenesis of CCI progression. After 8-14 days of standard drug therapy in patients with IS four Pl phenotypes was identified; from what - three phenotype receptors [ADP (<) Adrenaline (<) PAF (<)], [ADP (=) Adrenaline (=) PAF (=)], [ADP (>) Adrenaline (>) PAF (>)] that saved a their presence in the progression of vascular encephalopathy. Research of the basic phenotypes confirmed the possibility of interaction of ADP, epinephrine and PAF in improving of functional activity of Pl.