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脑血管痉挛是蛛网膜下腔出血(SAH)最严重的并发症之一,常引起严重局部脑组织缺血或迟发性缺血性脑损害,甚至导致脑梗死,是SAH病人致死和致残的重要原因,发病机制目前尚未明确。近年来研究认为:炎症反应在迟发性脑血管痉挛的发病机制中起重要作用,可能的机制包括全身炎症反应,白细胞与内皮细胞相互作用,各种细胞因子、黏附分子和信号转导通路的参与及某些炎症相关蛋白基因型改变等。本文对SAH后脑血管痉挛炎症机制作一综述。
Cerebral vasospasm is one of the most serious complication of subarachnoid hemorrhage (SAH), often causing severe local brain ischemia or delayed ischemic brain damage, and even lead to cerebral infarction, is the death and disability of SAH patients The important reason, the pathogenesis is not yet clear. In recent years, studies suggest that: inflammatory response plays an important role in the pathogenesis of delayed-onset cerebral vasospasm. Possible mechanisms include systemic inflammatory response, leukocyte-endothelial cell interaction, various cytokines, adhesion molecules and signal transduction pathways Participate in and some inflammation-related protein genotype changes. This article summarizes the inflammatory mechanisms of cerebral vasospasm after SAH.