阿替普酶溶栓治疗对急性脑梗死患者氧化应激相关因子水平和神经功能的影响

The effects of thrombolytic therapy with acipppet on oxidative stress factor level and neurological function in patients with acute cerebral infarction

目的分析阿替普酶溶栓治疗对急性脑梗死患者氧化应激相关因子水平和神经功能的影响。方法选取本院2016年5月-2018年5月收治的急性脑梗死患者60例,根据治疗方法不同分为对照组和观察组;对照组患者采用尿激酶溶栓治疗,观察组患者采用阿替普酶静脉溶栓治疗,分析2组患者治疗后的临床效果。结果治疗前2组患者大脑中动脉血流动力学指标水平、NIHSS评分比较无明显差异(P>0.05);治疗7d后观察组患者大脑中动脉收缩期峰值、舒张末期及平均流速高于对照组;治疗14、28d后NIHSS评分低于对照组(P<0.05)。治疗前2组患者8-OHdG、MDA、Ang-Ⅱ、CD62p、GMP-140、TNF-α水平比较无明显差异(P>0.05);治疗7d后观察组患者8-OHdG、MDA、Ang-Ⅱ、CD62p、GMP-140、TNF-α水平低于对照组(P<0.05)。观察组患者不良反应发生率为6.67%,对照组为16.67%,2组患者不良反应发生率比较无明显差异(P>0.05)。结论阿替普酶溶栓治疗可改善急性脑梗死患者的神经功能,其机制可能与降低氧化应激相关因子、Ang-Ⅱ、CD62p、GMP-140水平有关。

Objective To analyze the effects of thrombolytic therapy with acipppet on oxidative stress factor level and neurological function in patients with acute cerebral infarction.Methods Sixty patients with acute cerebral infarction admitted in our hospital from May 2016 to May 2018 were divided into control group and observation group according to different treatment methods.The patients in the control group were treated with aspirin orally,and the patients in the observation group were treated with intravenous thrombolytic therapy.Results There was no significant difference in NIHSS score between the two groups before treatment(P>0.05).After treatment the systolic peak,end-diastolic and mean flow velocity of the middle cerebral artery in the observation group were faster than those in the control group(P<0.05).Before the treatment there was no significant difference in the levels of 8-OHdG,MDA,Ang-Ⅱ and CD62 p,GMP-140,TNF-αbetween the two groups(P>0.05).After treatment the levels of 8-OHdG,MDA,Ang-Ⅱand CD62 p,GMP-140,TNF-αin the observation group were significantly lower than those in the control group(P<0.05).The adverse reaction rate was 6.67 in the observation group and 16.67 in the control group(P>0.05).Conclusion The neurologic function of patients with acute cerebral infarction could be improved after thrombolytic therapy with atropine,and the mechanism might be related to the reduction of the levels of oxidative stress factors,Ang-Ⅱ,CD62 p,GMP-140.