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目的 研究安替瑞丝方防治再狭窄的生化机制。方法 健康雄性新西兰白兔29只,随机分为假手术组(n=9)、模型组(n=9)、治疗组(n=11),采用兔右侧髂动脉进行球囊扩张加高脂饲养的方法,制作动脉狭窄模型,然后进行PTA治疗,并停用高脂饲养4周。观察治疗前后血清胆固醇(TC)、三酰甘油(TG)、组织纤溶酶原激活物(tPA)、纤溶酶原激活抑制物(PAI)、内皮素(ET)、一氧化氮(NO)水平的变化及各因素与再狭窄发生率的相关性。结果 模型组和对照组比较,疗程结束后两组TC分别为(482±205) mg%和(270±156) mg%(P<0.05);ET分别为(203±47) pg%和(138±25)pg%(P<0.001);TG、tPA、PAI、NO组间差异无统计学意义,而且再狭窄发生率只与ET水平呈正相关(P<0.05)。结论 安替瑞丝方能够通过降低血清TC和ET水平抑制再狭窄的发生。
Objective To study the biochemical mechanism of anti-restenosis with anti-restraint. Methods Twenty-nine male New Zealand white rabbits were randomly divided into sham-operated group (n=9), model group (n=9), and treatment group (n=11). Rabbits were subjected to balloon dilatation and hyperlipidemia using the right iliac artery. The method of feeding, making a model of arterial stenosis, followed by PTA treatment, and stopping high-fat feeding for 4 weeks. Observe serum cholesterol (TC), triglyceride (TG), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), endothelin (ET), and nitric oxide (NO) before and after treatment. Changes in levels and the correlation of various factors with the incidence of restenosis. Results Compared with the control group, the TCs of the two groups were (482±205) mg% and (270±156) mg% (P<0.05); the ET was (203±47) pg% and (138) respectively. ±25)pg% (P<0.001); There was no significant difference between TG, tPA, PAI and NO groups, and the incidence of restenosis was only positively correlated with ET levels (P<0.05). Conclusion Antolisone can inhibit restenosis by reducing the levels of serum TC and ET.