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目的:探讨二十碳五烯酸(EPA)与尼莫地平(nimodipine)对减轻动脉瘤性蛛网膜下腔出血后的脑血管痉挛的影响。方法:选70例接受开颅夹闭(craniotomy and clip)手术治疗的动脉瘤性蛛网膜下腔出血患者,随机分为对照组(n1=16),尼莫地平组(n2=26)和EPA组(n3=28)。对照组患者术后未特殊服用解痉药物,EPA组和尼莫地平组患者术后第4天开始口服1800mg/d剂量的EPA和尼莫地平120mg/d。观察脑血管迟发痉挛、脑梗死发生及术后一月随访的临床结果。结果:EPA和尼莫地平可以显著减少脑血管痉挛(n1group:36.1%,n2group:14.5%,P<0.05;n3group:13.8%,P<0.05)和脑血管痉挛引起的脑梗死的发生(n1group:26%,n2group:4.2%,P<0.01;n3group:3.5%,P<0.01),而EPA组和尼莫地平组1个月临床随访结果不良事件无明显差异。结论:EPA仅为减轻动脉瘤性蛛网膜下腔出血后的脑血管痉挛和脑梗死提供了一个治疗方向,但其具体机制仍需进一步研究。
Objective: To investigate the effects of eicosapentaenoic acid (EPA) and nimodipine on cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Methods: Seventy patients with aneurysmal subarachnoid hemorrhage undergoing craniotomy and clip surgery were randomly divided into control group (n1 = 16), nimodipine group (n2 = 26) and EPA Group (n3 = 28). Patients in the control group were given no antispasmodic drugs after the operation, and EPA and nimodipine 120 mg / d were orally administered to the patients in the EPA and nimodipine groups on day 4 postoperatively. To observe the clinical results of cerebrovascular delayed spasm, cerebral infarction and follow-up one month after operation. Results: EPA and nimodipine significantly reduced the incidence of cerebral infarction due to cerebral vasospasm (n1group: 36.1%, n2group: 14.5%, P <0.05; n3group: 13.8%, P <0.05) and cerebral vasospasm N2group: 4.2%, P <0.01; n3group: 3.5%, P <0.01). There was no significant difference in the adverse events of the 1-month clinical follow-up between the EPA group and the nimodipine group. Conclusion: EPA only provides a therapeutic direction for the reduction of cerebral vasospasm and cerebral infarction after aneurysmal subarachnoid hemorrhage. However, the specific mechanism needs further study.