Effect of midazolam on expression of adhession molecules on the platelet membrane surface in patients with coronary heart disease
- VernacularTitle:咪唑安定对冠心病患者外周静脉血血小板膜表面黏附分子表达的影响
- Author:
Ruoshan LIU
;
Xiaoming DENG
;
Wenzhong ZHU
- Publication Type:Journal Article
- Keywords:
Midazolam;
Blood platelets;
Cell adhesion molecules;
Coronary arteriosclerosis
- From:
Chinese Journal of Anesthesiology
1995;0(12):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of midazolam on expression of adhesion molecules on the platelet membrane surface in patients with coronary heart disease (CHD) .Methods Blood samples were taken from 10 healthy volunteers and 40 patients with CHD and anticoagulated with 3.8% sodium citrate. Platelet rich plasma (PRP) was obtained by centrifugation at 800 r/min for 8 min at room temperature. Ten volunteers served as control group (group E). The 40 patients with CHD were randomly divided into 4 groups ( n = 10 each) : group A, B, C and D. In group E and group A PRP was incubated without midazolam while in group B, C and D PRP was incubated with midazolam 100 (B) , 200 (C) and 400 ng?ml-1 (D) for 3 min. The inhibitory effect of midazolam on expression of CD154, CD41/61 and CD26p on the platelet membrane surface was determined by flow cytometry. Results The five groups were comparable with respect to age, sex (M/F ratio) , body weight, platelet count, bleeding and coagulation time. The expression of CD154, CD41/61 and CD62p on the platelet surface was significantly increased in patients with CHD. Midazolam 200 and 400 ng?ml-1 inhibited the expression of CD154, CD41/61 and CD62p on the platelet membrane surface in patients with CHD, whereas midazolam 100 ?g?ml-1 had no significant effect on CD154, CD41/61 and CD62p. Conclusion The expression of adhesion molecules on the platelet membrane surface is greater in patients with CHD than in healthy adults. Midazolam 200 and 400 ng?ml-1 can inhibit the expression of CD154, CD41/61 and CD62p on the platelet membrane surface.