Sensitivity of thrombocytes to the antiaggregation effect of prostacyclin was decreased in patients with dyscirculatory encephalopathy, which occurred in response to, at least, two reasons: a decrease in content of highly affinity receptors of prostacyclin on thrombocyte membranes and as a result of impairment in binding ability of the thrombocyte protein kinases. Combination of both these factors was also possible, which caused especially distinct impairments in the prostacyclin control of the thrombocyte functions.
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