Inflammatory cytokines in subarachnoid haemorrhage:: association with abnormal blood flow velocities in basal cerebral arteries
Inflammatory cytokines in subarachnoid haemorrhage:: association with abnormal blood flow velocities in basal cerebral arteries
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DOI：
10.1136/jnnp.70.4.534
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发表时间：
2001-04-01
影响因子：
11
通讯作者：
Hennerici, M
中科院分区：
文献类型：
--
作者：
Fassbender, K;Hodapp, B;Hennerici, M
在35例蛛网膜下腔出血（SAH）患者和对照组中，对炎性细胞因子（白细胞介素（IL）-1 β、IL-6和肿瘤坏死因子（TNF）-α）的蛛网膜下腔释放进行了表征，并将其与基底动脉并发血流动力学异常的发生和临床结局进行了比较。系列分析允许观察蛛网膜下腔这些关键炎症介质的亚急性反应特征。这种区室化的炎症宿主反应在时间和程度上与经颅多普勒超声记录的基底脑血管血流速度增加密切相关。此外，在临床结果较差的患者中，炎性细胞因子的鞘内分泌显著增加。总之，这些研究结果表明，过度区室化的炎症宿主反应在SAH后脑血管并发症的发病机制中起作用。
Subarachnoidal release of inflammatory cytokines (interleukin (IL)-1 beta, IL-6, and tumour necrosis factor (TNF)-alpha) was characterised in 35 patients with subarachnoid haemorrhage (SAH) and control subjects and compared with development of complicating haemodynamic abnormalities in basal cerebral arteries and clinical outcome. Serial analysis allowed the observation of a subacute response profile of these key mediators of inflammation in the subarachnoidal space. This compartmentalised inflammatory host response was closely associated in time and extent with development of increased blood flow velocities in the basal cerebral vessels as recorded by transcranial Doppler sonography. Moreover, intrathecal secretion of inflammatory cytokines was significantly increased in patients with poor clinical outcome. Together, these findings suggest a role of excessive compartmentalised inflammatory host response in pathogenesis of cerebrovascular complications after SAH.