[Mechanisms of changes in the sensitivity of platelets to prostacyclin in patients with cerebrovascular diseases].
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.
Akopov
S E
SE
Mkhitarian
G S
GS
Nikogosian
G A
GA
Gabrielian
E S
ES
D015121:6-Ketoprostaglandin F1 alpha / Q000494:pharmacology; D000328:Adult; D000527:Alprostadil / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002561:Cerebrovascular Disorders / Q000097:blood*; D000242:Cyclic AMP / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology; D011464:Epoprostenol / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D000242:Cyclic AMP; D000527:Alprostadil; D015232:Dinoprostone
O mekhanizmakh izmeneniia chuvstvitel'nosti trombotsitov k prostatsiklinu u bol'nykh s tserebrovaskuliarnymi zabolevaniiami.