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目的观察尿激酶溶栓及联合硫酸镁进行神经保护对急性脑梗死大鼠血中一氧化氮(NO)、内皮素(ET)水平的影响。方法应用光化学诱导法建立大鼠大脑中动脉闭塞(MCAO)模型,分为术后2 h、6 h 和10 h 干预组,每个时间点内再分为生理盐水组、尿激酶溶栓组、尿激酶联合硫酸镁组,另设假手术组,术后24 h 测定各组大鼠血中 NO、ET 含量。结果生理盐水组与尿激酶组 NO、ET 水平较假手术组明显升高,有显著性差异(P<0.01),两组之间于同时间点相比差异无显著性(P>0.05)。联合治疗能显著降低 NO、ET 水平,与同时间点的生理盐水组及尿激酶溶栓组相比差异显著(P<0.01或 P<0.05)。结论缺血后及尿激酶溶栓后大鼠血中 NO、ET 水平升高,参与脑缺血及再灌注损伤过程;镁剂可对抗 ET,清除 NO,起到神经保护作用。
Objective To observe the effect of urokinase thrombolysis combined with magnesium sulfate on the level of blood nitric oxide (NO) and endothelin (ET) in rats with acute cerebral infarction. Methods The middle cerebral artery occlusion (MCAO) model of rats was established by photochemical induction method and divided into 2 h, 6 h and 10 h postoperative intervention groups, and each time point was further divided into normal saline group, urokinase thrombolysis group, Urokinase combined with magnesium sulfate group, another set of sham-operated group, 24 h after operation to determine the content of NO and ET in blood of rats in each group. Results The levels of NO and ET in normal saline group and urokinase group were significantly higher than those in sham operated group (P <0.01). There was no significant difference between the two groups at the same time point (P> 0.05). Combination therapy can significantly reduce NO, ET levels, compared with the same time points in the saline group and urokinase thrombolysis group, the difference was significant (P <0.01 or P <0.05). Conclusion After ischemia and urokinase thrombolytic therapy, NO and ET levels in blood of rats are increased, which may be involved in the process of cerebral ischemia and reperfusion injury. Magnesium can antagonize ET and clear NO, and play a neuroprotective role.