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目的观察丁苯酞联合尿激酶治疗急性脑梗死的疗效和安全性。方法将46例经DWI、PWI证实存在半暗带的急性脑梗死患者,随机分为治疗组(丁苯酞+尿激酶)23例、对照组(尿激酶组)23例、对2组病例在治疗前、治疗后进行NIHSS评分、检测2组超氧化物歧化酶(SOD)、丙二醛(MDA)值并记录患者的APTT值变化,观察颅内出血等并发症的发生情况。结果经治疗后,2组患者的NIHSS评分均比治疗前明显好转,且治疗组优于对照组,差异有统计学意义(P<0.01);治疗组血清SOD活性明显升高,MDA水平显著下降(P<0.05);2组的APTT值变化差异无统计学意义;经临床观察2组患者均无继发颅内出血发生。结论丁苯酞可能通过抑制自由基的生成、保护线粒体功能,进而改善神经功能缺损,且与尿激酶联用时未影响凝血功能及增加颅内出血的风险。
Objective To observe the efficacy and safety of butylphthalide combined with urokinase in the treatment of acute cerebral infarction. Methods Forty-six patients with acute cerebral infarction confirmed by penumbra and PWI were randomly divided into treatment group (butylphthalide + urokinase) and control group (urokinase group), 23 cases were divided into two groups NIHSS scores were measured before treatment and after treatment. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in 2 groups were detected and APTT values were recorded. The complication of intracranial hemorrhage and other complications were observed. Results After treatment, the NIHSS scores of the two groups were significantly improved compared with that before treatment, and the treatment group was superior to the control group, the difference was statistically significant (P <0.01); the serum SOD activity was significantly increased and MDA level was significantly decreased (P <0.05). There was no significant difference in APTT between the two groups. There was no secondary intracranial hemorrhage in the two groups after clinical observation. Conclusion Butylphthalide may protect the function of mitochondria by inhibiting the formation of free radicals and thus improve the neurological deficits. However, combination with urokinase does not affect the coagulation function and increase the risk of intracranial hemorrhage.