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蛛网膜下腔出血后的液体代谢途径。

Fluid metabolic pathways after subarachnoid hemorrhage.

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Department of Neurosurgery and State Key Laboratory of Trauma, Burn and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

出版信息

J Neurochem. 2022 Jan;160(1):13-33. doi: 10.1111/jnc.15458. Epub 2021 Jul 12.

DOI:10.1111/jnc.15458
PMID:34160835
Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating cerebrovascular disease with high mortality and morbidity. In recent years, a large number of studies have focused on the mechanism of early brain injury (EBI) and delayed cerebral ischemia (DCI), including vasospasm, neurotoxicity of hematoma and neuroinflammatory storm, after aSAH. Despite considerable efforts, no novel drugs have significantly improved the prognosis of patients in phase III clinical trials, indicating the need to further re-examine the multifactorial pathophysiological process that occurs after aSAH. The complex pathogenesis is reflected by the destruction of the dynamic balance of the energy metabolism in the nervous system after aSAH, which prevents the maintenance of normal neural function. This review focuses on the fluid metabolic pathways of the central nervous system (CNS), starting with ruptured aneurysms, and discusses the dysfunction of blood circulation, cerebrospinal fluid (CSF) circulation and the glymphatic system during disease progression. It also proposes a hypothesis on the metabolic disorder mechanism and potential therapeutic targets for aSAH patients. Cover Image for this issue: https://doi.org/10.1111/jnc.15384.

摘要

颅内动脉瘤性蛛网膜下腔出血(aSAH)是一种具有高死亡率和高发病率的毁灭性脑血管疾病。近年来,大量研究集中在 aSAH 后早期脑损伤(EBI)和迟发性脑缺血(DCI)的机制上,包括血管痉挛、血肿的神经毒性和神经炎症风暴。尽管付出了相当大的努力,但在 III 期临床试验中,没有新型药物显著改善患者的预后,这表明需要进一步重新审视 aSAH 后发生的多因素病理生理过程。复杂的发病机制反映在 aSAH 后神经系统能量代谢的动态平衡被破坏,从而阻止了正常神经功能的维持。这篇综述重点关注中枢神经系统(CNS)的液体代谢途径,从破裂的动脉瘤开始,并讨论了在疾病进展过程中血液循环、脑脊液(CSF)循环和胶状淋巴系统的功能障碍。它还提出了一个关于 aSAH 患者代谢紊乱机制和潜在治疗靶点的假设。本期封面图片:https://doi.org/10.1111/jnc.15384.

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