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目的:探讨急性脑梗死早期应用奥扎格雷治疗的临床疗效及对患者血浆超敏C-反应蛋白(hs-CRP)和血小板聚集率的影响。方法:将80例急性脑梗死患者随机分为对照组和奥扎格雷组。入院后均予以相同的抗高血压、降颅压、营养脑细胞及对症处理等治疗。奥扎格雷组在以上治疗基础上加用奥扎格雷注射液80mg静脉滴注,2次/d,连用1周。观察治疗前后血浆hs-CRP和血小板聚集率的变化,并进行临床神经功能缺损评价及不良反应的观察。结果:两组患者治疗1周后,患者血浆hs-CRP和血小板聚集率均明显下降,与治疗前比较有明显统计学差异(P<0.01或P<0.05),且奥扎格雷组下降幅度更明显(P<0.05);同时神经功能缺损评分均明显下降,与治疗前比较有明显统计学差异(P<0.01或P<0.05),且奥扎格雷组下降幅度更明显(P<0.05)。奥扎格雷组治疗期间无明显不良反应。结论:急性脑梗死早期应用奥扎格雷治疗的疗效确切,能明显改善脑梗死部位缺血缺氧和缺损神经功能,安全性好。作用机制与降低血浆hs-CRP和血小板聚集率,减轻炎症反应和抑制血小板聚集有关。
Objective: To investigate the clinical efficacy of ozagrel in the early stage of acute cerebral infarction and its effect on plasma hs-CRP and platelet aggregation rate. Methods: Eighty patients with acute cerebral infarction were randomly divided into control group and ozagrel group. After admission to the same anti-hypertensive, intracranial pressure, nutritional brain cells and symptomatic treatment. Ozagrel group on the basis of the above treatment plus Ozagrel 80mg intravenous infusion, 2 times / d, once a week. The changes of plasma hs-CRP and platelet aggregation rate before and after treatment were observed, and clinical neurological deficit evaluation and adverse reaction were observed. Results: The levels of plasma hs-CRP and platelet aggregation in two groups were significantly decreased after one week of treatment, which were significantly different from those before treatment (P <0.01 or P <0.05), and decreased more in the ozagrel group (P <0.05). At the same time, the score of neurological deficit decreased significantly compared with that before treatment (P <0.01 or P <0.05), and decreased more significantly in ozagrel group (P <0.05). Ozagrel group no significant adverse reactions during treatment. Conclusion: Early application of ozagrel in patients with acute cerebral infarction has definite curative effect, which can obviously improve ischemic, hypoxic and deficient neurological function of cerebral infarction, and has good safety. Mechanism of action and reduce plasma hs-CRP and platelet aggregation rate, reduce inflammation and inhibition of platelet aggregation.