银杏二萜内酯葡胺注射液对急性脑梗死合并多发性颅内动脉狭窄患者血清NO、ET-1的影响及疗效观察

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目的观察银杏二萜内酯葡胺注射液对急性脑梗死合并多发性颅内动脉狭窄患者血清NO、ET-1的影响及疗效观察。方法将101例急性脑梗死合并多发性颅内动脉狭窄的住院患者随机分成观察组50例、对照组51例,两组分别予西医常规治疗,观察组加用银杏二萜内酯葡胺注射液,对照组加用舒血宁注射液。治疗前、后抽取静脉血,应用ELISA法检测ET-1的表达,用硝酸还原酶法检测NO的表达。并以神经功能缺损程度评分(NIHSS)减少率作为疗效判断标准。结果治疗2W后两组ET-1水平、NIHSS评分均较治疗前明显下降,而NO水平均较治疗前明显升高,但观察组ET水平、NIHSS评分的下降值明显高与对照组,而NO水平上升值明显高于对照组,且差异具有统计学意义(P<0.05)。结论银杏二萜内酯葡胺注射液可能通过更有效地纠正血清中ET-1和NO比例失衡这一作用机制,改善患者临床症状,维持内皮功能稳定,延缓动脉粥样硬化的发生及进展。 Objective To observe the effect of ginkgo diterpene lactone meglumine injection on serum NO and ET-1 in patients with acute cerebral infarction complicated with multiple intracranial arterial stenosis and its therapeutic effect. Methods A total of 101 hospitalized patients with acute cerebral infarction complicated with multiple intracranial arterial stenosis were randomly divided into observation group (n = 50) and control group (n = 51). The two groups were given routine western medicine. The observation group was given ginkgo diterpene lactone meglumine injection , Control group with Shuxuening injection. Venous blood was drawn before and after treatment. The expression of ET-1 was detected by ELISA and the expression of NO was detected by nitrate reductase method. And the rate of neurological deficit score (NIHSS) reduction as a criterion for efficacy. Results After 2 weeks of treatment, the levels of ET-1 and NIHSS in the two groups were significantly decreased compared with those before treatment, while the levels of NO in the two groups were significantly higher than those before treatment. However, the levels of ET in the observation group and the NIHSS scores in the observation group were significantly lower than those in the control group The level of rise was significantly higher than the control group, and the difference was statistically significant (P <0.05). Conclusions Ginkgolide diterpene lactone meglumine injection may improve the clinical symptoms, maintain the endothelial function and delay the occurrence and progression of atherosclerosis by more effectively correcting the mechanism of imbalance of ET-1 and NO in serum.
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