Aneurysmal subarachnoid hemorrhage (SAH) remains a serious cerebrovascular disease. Even if SAH patients survive the initial insults, delayed cerebral ischemia (DCI) may occur at 4 days or later post-SAH. DCI is characteristics of SAH, and is considered to develop by blood breakdown products and inflammatory reactions, or secondary to early brain injury, acute pathophysiological events that occur in the brain within the first 72 hours of aneurysmal SAH. The pathology underlying DCI may involve large artery vasospasm and/or microcirculatory disturbances by microvasospasm, microthrombosis, dysfunction of venous outflow and compression of microvasculature by vasogenic or cytotoxic tissue edema. Recent clinical evidence has shown that large artery vasospasm is not the only cause of DCI, and that both large artery vasospasm-dependent and -independent cerebral infarction causes poor outcome. Animal studies suggest that mechanisms of vasospasm may differ between large artery and arterioles or capillaries, and that many kinds of cells in the vascular wall and brain parenchyma may be involved in the pathogenesis of microcirculatory disturbances. The impairment of the paravascular and glymphatic systems also may play important roles in the development of DCI. As pathological mediators for DCI, glutamate and several matricellular proteins have been investigated in addition to inflammatory molecules. Glutamate is involved in excitotoxicity contributing to cortical spreading ischemia and epileptic activity-related events. Microvascular dysfunction is an attractive mechanism to explain the cause of poor outcomes independently of large cerebral artery vasospasm, but needs more studies to clarify the pathophysiologies or mechanisms and to develop a novel therapeutic strategy.

中文翻译：

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动脉瘤性蛛网膜下腔出血后迟发性脑缺血的脑血管病理生理。

动脉瘤性蛛网膜下腔出血（SAH）仍然是一种严重的脑血管疾病。即使 SAH 患者在最初的损伤中幸存下来，延迟性脑缺血 (DCI) 也可能在 SAH 后 4 天或更晚发生。DCI 是 SAH 的特征，被认为是由血液分解产物和炎症反应发展而来，或继发于早期脑损伤、动脉瘤性 SAH 最初 72 小时内发生在大脑中的急性病理生理事件。DCI 的病理可能涉及大动脉血管痉挛和/或微血管痉挛引起的微循环障碍、微血栓形成、静脉流出功能障碍和血管源性或细胞毒性组织水肿对微血管系统的压迫。最近的临床证据表明，大动脉血管痉挛并不是 DCI 的唯一原因，并且大动脉血管痉挛依赖性和非依赖性脑梗塞都会导致不良结果。动物研究表明，大动脉和小动脉或毛细血管的血管痉挛机制可能不同，血管壁和脑实质中的多种细胞可能参与微循环障碍的发病机制。血管旁和淋巴系统的损伤也可能在 DCI 的发展中发挥重要作用。除了炎症分子外，还研究了作为 DCI 的病理介质的谷氨酸盐和几种基质细胞蛋白。谷氨酸参与导致皮层扩散缺血和癫痫活动相关事件的兴奋性毒性。