ABSTRACT
Objective To evaluate the effect of midazolam on platelet activation in patients with coronary heart disease (CHD) .Methods Brachial venous blood samples 5 ml drawn from 10 healthy adult volunteers and 40 patients with CHD were anticongulated with 3.8 % sodium citrate. Platelet rich plasma (PRP) 3 ml was obtained by centrifngation at 800 rpm for 8 min. Experiment Ⅰ : Ten portions of PRP from healthy adult volunteers served as control group with 1 ml for each (group ⅠC, n = 10). Forty portions of PRP from patients with CHD were randomly divided into 4 groups (n = 10 each): ⅠM0, ⅠM1,ⅠM2 and ⅠM3. In group ⅠC and ⅠM0, midazolam was not added while in group ⅠM1 , ⅠM2 and ⅠM3, midazolam was added with the final concentration at 100, 200 and 400 ng/ml respectively and the PRPs were then incubated for 3 min. The platelet aggregation rote was determined using turbidimetric method. Experiment Ⅱ : After the remaining PRP was eentrifnged at 2000 r/ rain for 5 min, washed platelets (WPs) were obtained. Ten portions of WPs from healthy adult volunteers served as control group with 1 ml for each (group ⅡC, n = 10). Forty portions of WPs from patients with CHD were randomly divided into 4 groups (n = 10 each) : ⅡM0, ⅡM1, ⅡM2 and ⅡM3· In group ⅡC and ⅡM0, midazolam was not added while in group Ⅱ<m1>, ⅡM2 and ⅡM3, midazolam was added with the final concentration at 100, 200 and 400 ng/ml respectively and the WPs were then incubated for 3 min. The content of platelet cAMP and were measured by enzyme immunoassay. Results Platelet aggregation rate was significantly higher in group ⅠM0 than in group ⅠC(P<0.01). Compared with groupⅠM0, platelet aggregation rate was significantly decreased in group ⅠM2 and ⅠM3(P<0.01) but there was no significant change in group ⅠM1 (P >0.05). The content of platelet cAMP was significantly decreased while the level of TXB2 was significantly increased in group ⅡM0 as compared with group ⅡC (P < 0.01). Compared with group Ⅱ M0, the content of platelet cAMP was significantly increased (P <0.05 or 0.01) while the level of TXB2 was significantly decreased in group ⅡM2 and ⅡM3(P< 0.01), but there was no significant change in group ⅡM1 (P > 0.05). Conclusion Midazolam 200 and 400 ng/ml can inhibit the platelet activation through increasing the content of platelet cAMP and reducing the production of TXA2 in vitro.
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.
ABSTRACT
Objective:To investigate changes of platelets and coagulation function in patients undergoing cardiac valvular replacement surgery during cardiopulmonary bypass(CPB).Methods: Thirty patients scheduled for elective cardiac valvular replacement were equally randomlized to 2 groups: control group and propofol group. In control group anesthesia was induced with midazolam 0.05 mg?kg -1,fentanyl 0.01 mg?kg -1 and vecuronium 0.1-0.2 mg?kg -1, and maintained with isoflurane,fentanyl and vecuronium. In propofol group anesthesia was induced with midazolam 0.05 mg?kg -1,fentanyl 0.005-0.01 mg?kg -1,propofol 1.5 mg?kg -1 and vecuronium 0.1-0.2 mg?kg -1, and propofol 4-5 mg?kg -1?h -1 was administered during operation with isoflurane,fentanyl and vecuronium. Blood samples were taken from jugular vein to assay SonACT, clot rate and platelet function with Sonoclot ananlysis, and to measure platelet count, PT and APTT before anesthesia, 5 min after induction,before CPB,10 min after CPB and at the end of operation.Results: Compared with those before anesthesia, PF, clot rate, platelet count, PT and APTT in both groups significantly decreased 10 min after CPB and at the end of operation(P
