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动脉瘤性蛛网膜下腔出血后血管痉挛患者脑脊液中白细胞介素-1β和白细胞介素-6水平升高。

Increase of the IL-1 beta and IL-6 levels in CSF in patients with vasospasm following aneurysmal SAH.

作者信息

Hendryk Stanislaw, Jarzab Barbara, Josko Jadwiga

机构信息

Department of Neurosurgery and Neurotraumatology, Silesian Medical University, Bytom, Poland.

出版信息

Neuro Endocrinol Lett. 2004 Feb-Apr;25(1-2):141-7.

Abstract

Cytokines play a key role in mutual influence of the immunological, endocrine and CNS systems. It has been proven that proinflammatory ILs may intensify the cascade of biochemical changes in ischemic brain damage. Vasospasm, which may accompany SAH and often coexists with symptoms of DINDs, is the cause of ischemic changes in the brain. It is thought that immunological mechanisms may be one of the causes of degenerative-productive changes in vessel walls, in delayed vasospasm following SAH, which lead to substantial vasospasm and in consequence too cerebral ischemia. In the randomly selected group of patients, who underwent surgical treatment after aneurysmal SAH, we determined the concentration of IL-1 beta and IL-6 in CSF in the periods between Days 0 to 3; 4 to 7; and 8 to 15 after the occurrence of SAH. The presence and dynamics of development of vasospasm were assessed on the basis of increasing DINDs as well as CT and cerebral angiography. We examined the concentrations of ILs in CSF using radioimmunological methods, applying commercially available tests for their assessment. We found that in the period between 8 and 15 days after SAH, in increasing delayed vasospasm and DINDs, here is a statistically significant increase concentration of IL-1 beta in CSF (105.4 +/- 46.9 pg x ml-1; p<0.005), and no significant changes in patients without vasospasm and neurological deficits. On the other hand, we noted a statistically significant increase concentration of IL-6 in CSF (4802 +/- 1170 ng x ml-1; p<0.05) only in the acute phase after SAH (Days 0-3) in patients in poor clinical condition, in whom delayed vasospasm and cerebral ischemia developed later. This increase of ILs level in CSF is probably related to the intensity of the SAH, and secondarily aggravates the vasospasm and ischemic changes in the brain.

摘要

细胞因子在免疫、内分泌和中枢神经系统的相互影响中起关键作用。业已证实,促炎白细胞介素可能会加剧缺血性脑损伤中的一系列生化变化。血管痉挛可能伴随蛛网膜下腔出血(SAH)出现,且常与延迟性缺血性神经功能障碍(DINDs)的症状并存,是脑部缺血性变化的原因。人们认为免疫机制可能是SAH后延迟性血管痉挛中血管壁退行性 - 增生性变化的原因之一,这种变化会导致严重的血管痉挛,进而导致脑缺血。在随机选取的一组动脉瘤性SAH后接受手术治疗的患者中,我们测定了SAH发生后第0至3天、第4至7天以及第8至15天期间脑脊液中白细胞介素 - 1β(IL - 1β)和白细胞介素 - 6(IL - )的浓度。基于DINDs的增加以及CT和脑血管造影来评估血管痉挛的存在和发展动态。我们使用放射免疫方法并应用市售检测试剂盒来检测脑脊液中白细胞介素的浓度。我们发现,在SAH后的第8至15天期间,随着延迟性血管痉挛和DINDs的增加,脑脊液中IL - 1β的浓度有统计学意义的显著升高(105.4±46.9 pg×ml - 1;p<0.005),而在没有血管痉挛和神经功能缺损的患者中无显著变化。另一方面,我们仅在临床状况较差且后期发生延迟性血管痉挛和脑缺血的患者SAH急性期(第0 - 3天)发现脑脊液中IL - 6的浓度有统计学意义的显著升高(4802±1170 ng×ml - 1;p<0.05)。脑脊液中白细胞介素水平的这种升高可能与SAH的严重程度有关,继而加重脑部的血管痉挛和缺血性变化。

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