[Interaction of the Humoral Agonist During the Platelets Activation in Patients with Chronic Cerebral Ischemia].
OBJECTIVE
The aim of the study was to determine the effect of the standard drug therapy of 95 patients with chronic cerebral ischemia (CCI) on the functional status of platelets as possible participants of microcirculation of the brain.


METHODS
Platelets were isolated from peripheral blood by centrifugation and examined at 24 hours after initiation of standard medical therapy including aspirin (100 mg). The cells were stimulated in vitro using adenosine diphosphate (ADP), epinephrine, platelet activating factor (PAF) and serotonin in an effective concentration (EC50) inducing in healthy individuals platelet aggregation in the range of 50 ± 5%. A study of platelet aggregation was carried out on aggregometer Chrono-Log (USA).


RESULTS
Research included 95 patients with CCI 1-2 Stage--82 patients taking antiplatelet and antihypertensive drugs before hospitalization (main group), 13--did not receive these drugs during 7 days prior to hospitalization (comparison group). After start conservative treatment, only ADP induced platelet aggregation, which was similar (p > 0.05) with values in healthy individuals. The pharmacological inhibition of the functional activity of platelets other investigated agonists reproduced hyporesponsiveness of platelets. Against this background, in 34 (41.5%) patients at 24 hours after initiation of therapy occurred potentiation effects of PAF and epinephrine in the test in vitro; whereas the summation of the effects of serotonin and epinephrine on platelets was detected in 12 (14.6%) patients. The basis of this phenomenon may be strengthening effect of ADP secreted from dense-granules, additional stimulation by Gi-protein signaling system by epinephrine and Gq-protein by the action of PAF and serotonin.


CONCLUSIONS
Response to the combined action of platelet agonists may be predictor of the risk of thrombogenesis at CCI.
E F
EF
Barinov
S
S
Mamedaliyeva
T A
TA
Tverdokhleb
D000244:Adenosine Diphosphate / Q000378:metabolism; D000328:Adult; D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000502:physiology*; D001921:Brain / Q000098:blood supply*; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology; D002908:Chronic Disease; D004837:Epinephrine / Q000378:metabolism; D005260:Female; D006801:Humans; D020767:Intracranial Thrombosis / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D008833:Microcirculation; D010972:Platelet Activating Factor / Q000378:metabolism; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism
D010972:Platelet Activating Factor; D010975:Platelet Aggregation Inhibitors; D012701:Serotonin; D000244:Adenosine Diphosphate; D001241:Aspirin; D004837:Epinephrine