Calcium antagonists are widely used in the clinical treatment of ischemic cerebrovascular disease because of their vascular and neuroprotective effects. Nimodipine, a typical calcium antagonist, can cross the blood-brain barrier and act selectively at neurons and blood vessels of target tis-sues, thus exerting neuroprotective effects. The aim of the present study was to explore the hot spots and future trends of research on the neuroprotective effects of nimodipine. We retrieved 425 articles on the neuroprotective effects of nimodipine that were indexed in the Web of the Science database between 2000 and 2014. The retrieved articles were analyzed using document analysis reporting and the derived information function in the Web of Science, and the infor-mation visualization software CiteSpace III. The reference co-citation network was plotted, and the high frequency key words in these publications were used to analyze the research fronts and development trends for nimodipine neuroprotection. According to these co-citation clusters, the research front of nimodipine neuroprotection is the use of randomized controlled trials to study nimodipine intervention of subarachnoid hemorrhage. Using time zone view analysis on hot spots labeled with a key word, the areas of interest in the ifeld of nimodipine neuroprotection are nimodipine pharmacology and therapeutics, blood-brain barrier, trials, and anti-angiospasm.

钠通道Na(v)1.6与缺血性脑损伤

目的 通过观察大鼠缺血脑组织中Na(v)1.6表达探讨Na(v)1.6与缺血性脑损伤的关系.方法 线栓法制作大鼠脑缺血模型,168只SD大鼠分为假手术组、脑缺血组和钠通道阻滞剂-riluzole、钙通道阻滞剂-nimodipine治疗组.大鼠脑缺血后6h、1d、2d、3d取材,应用免疫组化检测Na(v)1.6表达,荧光法检测钙离子浓度,氯化三苯四唑染色检测脑梗死体积.结果 Na(v)1.6在脑缺血后6h～1d表达上调,2～3d表达下调；相同时间点nimodipine治疗组与缺血组相比较,Na(v)1.6表达变化不明显；riluzol治疗组Na(v)1.6表达变化明显,差异具有显著性(P＜0.05).riluzol治疗组和nimodipine治疗组钙离子浓度、脑梗死体积均比缺血组降低,riluzol治疗组降低明显,差异具有显著性(P＜0.05).结论 钠离子内流发生在脑缺血的早期阶段；脑缺血后Na(v)1.6表达上调,抑制Na(v)1.6表达可以减轻脑缺血损伤,Na(v)1.6参与了缺血性脑损伤.

Objective: To determine the efficacy and safety of early intervention with nimodipine treatment in diffuse axonal injury.Methods: Based on the characteristic radiological signs and criteria for diffuse axonal injury (DAI), 89patients with the diagnosis of DAI were enrolled in this randomized, double-blind, placebo-controlled trial. Results: Nimodipine proved to be safe and well tolerated. With TCD sonography we found that there was a higher incidence of cerebral vasospasm in this series (38.2%). Overall, Nimodipine produced a better clinical result than placebo, but there was no statistically significant difference in favorable outcome at 3 months after injury (P ＝ 0.11 ) between the two groups. A trend toward a favorable effect was suggested by the analyses in two small subgroups, either in the patients suffering from clinical Grade Ⅲ DAI (P ＝ 0.04), or in those with the TCDevidence of cerebral vasospasm during clinical observation (P ＝ 0.049).Conclusions: We postulate that a clinically valuable benefit is possible with nimodipine treatment in DAI patients. However, the effects on outcome should be verified by further controlled study.