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机构地区:[1]武汉科技大学医学院生理学系,湖北武汉430065 [2]襄阳市中心医院内科
出 处:《湖北科技学院学报(医学版)》2012年第5期388-391,共4页Journal of Hubei University of Science and Technology(Medical Sciences)
摘 要:目的观察替罗非班在颅内动脉狭窄实施支架置入术中的临床疗效及可能机制。方法 80例颅内动脉支架置入术患者随机分为对照组和替罗非班组,每组40例。随访两组患者主要脑血管事件和出血并发症,测定治疗前后患者血浆中C-反应蛋白(CRP)及IL-6评价体内炎症水平,检测PBMC中循环内皮细胞(CECs)数目评价内皮细胞受损程度。结果替罗非班组术后1、3和6个月mRS评分和BI评分均较对照组显著改善,差异有统计学意义(P<0.05);术后两组患者血浆中CRP和IL-6水平均较术前显著增高(P<0.01),替罗非班组术后6个月CRP水平较对照组显著降低(P<0.05),替罗非班组术后1周CECs数量较对照组水平显著降低(P<0.05)。结论替罗非班明显提高支架置入术治疗颅内动脉狭窄的临床疗效,其机制可能与其具有内皮细胞保护和抗炎作用有关。Objective To observation of intracranial artery bracket implantation of intracoronary applica- tion of platelet glycoprotein (GP) Ⅱ b/Ⅲ a receptor antagonist for the efficacy of tirofiban. Methods 80 pa- tients with intracranial artery stent placement were randomly divided into two groups, 40 cases of tirofiban group while the control group were 40 cases. The patients in control group were administered clopidogrel (75mg/d) and aspirin tablets (100mg/d) 3 days before surgery, systemic heparin was took for anticoagulation in surgery, clopidogrel (75mg/d) were administered for 6 months and aspirin tablets (100mg/d) were administered for long term. The patients in tirofiban group were continuous intravenous administered tirofiban (0.15 μg/kg/min) in 36 hours in surgery, but other therapeutic treatments were the same to those in control group. Modified Rankin Scale ( mRS ) and Barthel Index (BI) score were observed before surgery, 1,3 and 6 months after sur- gery , respectively. Circulating endothelial cells (CECs) number, plasma C-reactive protein (CRP) and IL-6 levels were detected. Results mRS score and BI scores in Tirofiban group at 1,3 and 6 months were significantly improved compared with the control group;CEC, CRP and IL-6 levels after surgery were significantly higher than those before surgery, but the tirofiban group were significantly reduced when compare with the control group. Conclusion Tirofiban significantly improved stenting for intracranial arterial stenosis in the clinical effi- cacy, its mechanism is partly due to reducing the endothelial cells (CEC) injury, C-reactive protein (CRP) and IL-6.
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