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中华脑血管病杂志(电子版) ›› 2026, Vol. 20 ›› Issue (04) : 351 -358. doi: 10.3877/cma.j.issn.1673-9248.2026.04.001

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急性缺血性脑卒中无效再通的研究进展及脑保护新策略
张爽, 谢琦(), 杨清武()   
  1. 400037 重庆,陆军军医大学第二附属医院神经内科
  • 收稿日期:2026-07-03 出版日期:2026-08-01
  • 通信作者: 谢琦, 杨清武
  • 基金资助:
    国家自然科学基金国际(地区)合作与交流项目(82320108006)

Research advances and novel neuroprotective strategies of futile recanalization in acute ischemic stroke

Shuang Zhang, Qi Xie(), Qingwu Yang()   

  1. Department of Neurology, the Second Affiliated Hospital of Army Medical University, Chongqing 400037, China
  • Received:2026-07-03 Published:2026-08-01
  • Corresponding author: Qi Xie, Qingwu Yang
引用本文:

张爽, 谢琦, 杨清武. 急性缺血性脑卒中无效再通的研究进展及脑保护新策略[J/OL]. 中华脑血管病杂志(电子版), 2026, 20(04): 351-358.

Shuang Zhang, Qi Xie, Qingwu Yang. Research advances and novel neuroprotective strategies of futile recanalization in acute ischemic stroke[J/OL]. Chinese Journal of Cerebrovascular Diseases(Electronic Edition), 2026, 20(04): 351-358.

血管内取栓使得急性缺血性脑卒中(AIS)的治疗方式发生根本性的改变。然而,在目前的临床实践中还存在着一个突出的难题,即大约一半的患者虽然成功再通了堵塞的血管,但是神经功能并没有得到预期的改善,这种情况被称为无效再通。近些年来,脑保护药物同再通治疗联合使用给无效再通带来了新希望。尤其是免疫调节剂联合血管再通治疗可以减轻缺血再灌注损伤,降低发生无效再通的风险,给临床提供了新的干预策略。因此,本文从无效再通的关键机制和最新进展入手,用“血管-免疫-神经网络”的思路串联起脑保护干预措施,试图为破解这一难题、改善AIS患者远期预后提供理论上的借鉴。

Endovascular treatment has been fundamentally transformed the management of acute ischemic stroke (AIS). However, a prominent clinical challenge persists: almost half of the patients who have achieved successful recanalization of the occluded vessel fail to achieve the expected neurological improvement, a phenomenon termed "futile recanalization". In recent years, the combination of neuroprotective drugs with recanalization therapy has offered some new hope for this issue. Notably, combining immunomodulators with revascularization has shown potential to mitigate ischemia-reperfusion injury and reduce the risk of futile recanalization, providing novel clinical intervention strategies. Therefore, this review synthesizes the basic mechanisms of futile recanalization and new progress in this field. By employing a "vascular-immune-neural network" model to integrate various neuroprotective therapies, we aim to provide theoretical support for overcoming this challenge of AIS and improving the long-term prognosis of AIS patients.

图1 急性缺血性脑卒中(AIS)免疫反应全景概览(仅展示部分重要的要素)。①为脑血管闭塞之后,坏死的神经元会释放出抗原以及损伤相关的分子模式,活化的免疫细胞便会向体循环释放出促炎细胞因子和趋化因子;②为在趋化信号的作用下,外周和骨髓来源的固有免疫细胞被募集到脑实质中,同时骨髓开始髓系前体细胞的代偿性释放,以弥补外周淋巴器官的消耗;③为随着神经元凋亡加重、神经炎症的发展,中枢神经免疫通路(神经递质的释放等)被激活,使淋巴细胞凋亡或者使淋巴细胞迁移到骨髓中,从而造成脾脏和胸腺萎缩;④为进入AIS慢性期以后,淋巴细胞一直浸润在中枢神经系统的实质里,骨髓里的T细胞又回到循环中去,逐渐重建外周淋巴器官
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