噻氯匹定抗心肌缺血的疗效及其机制  

Therapeutic effects of ticlidine on myocardial ischemia and its mechanism

作　　者：何作云[1] 于学军[1] 文芳[1] 

机构地区：[1]第三军医大学附属新桥医院心血管内科

出　　处：《第三军医大学学报》1998年第1期24-26,共3页Journal of Third Military Medical University

基　　金：国家自然科学基金

摘　　要：目的：探讨噻氯匹定增强地尔硫和５－单硝酸异山梨醇酯抗心肌缺血的疗效及其机制。方法：不稳定型心绞痛常规治疗组（ＣＧ）及合用噻氯匹定组（ＴＧ）各２０例，检查其治疗前、后心肌缺血总负荷和缺血性ＳＴ段事件次数；血小板的粘附率、聚集率和血小板计数；血小板膜ＧＰⅠｂ、ＧＰⅡｂ和ＧＰⅢａ。结果：用药４周时，ＴＧ中心肌缺血明显改善；血小板的粘附和聚集功能基本恢复正常，ＧＰⅠｂ相对含量明显降低，血小板计数明显增加，然而后两项指标未恢复正常（Ｐ＜０．０５）；尽管ＣＧ中心肌缺血亦有一定程度的改善，但对血小板计数、粘附和聚集功能以及ＧＰⅠｂ无明显的影响。结论：噻氯匹定具有增强抗心肌缺血的作用，抑制血小板的活性是其主要的机制之一。Objective: To investigate the enhancement of the therapeutic effects of diltiazem and isosorbide5mononitrate (CG) on myocardial ischemia by ticlidine in patients with unstable angina. Methods: Before and after the administration of the first two agents in the control group (CG, n=20) and all the three agents in the treated group (TG, n=20) respectively, the following indices were measured: 1) total ischemic burden (TIB) and counts of ischemic events; 2) adhesive rate, aggregation rate and counts of the platelet; 3) platelet membrane glycoproteins Ib (GPIb), IIb (GPIIb) and IIIa (GPIIIa). Results: In TG, parameters of myocardial ischemia were markedly improved, adhesive rate and aggregation rate of the platelet fundamentally recovered, relative counts of GPIb significantly declined and counts of the platelet increased but the last two indices still abnormal (P<0.05). In CG, myocardial ischemia was alleviated to some extent but no significant changes of other indices were found. Conclusion: Ticlidine can enhance the antimyocardial ischemic effects of other two agents. The mechanism of which is the inhibition of platelet activity.

关 键 词：噻氯匹定 血小板 心肌缺血 血小板活化 疗效 

分 类 号：R542.2[医药卫生—心血管疾病]