Cerebrospinal fluid interleukin-1 receptor antagonist and tumor necrosis factor-alpha following subarachnoid hemorrhage
Cerebrospinal fluid interleukin-1 receptor antagonist and tumor necrosis factor-alpha following subarachnoid hemorrhage
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DOI：
10.3171/jns.1997.87.2.0215
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发表时间：
1997-08-01
影响因子：
4.1
通讯作者：
Andersson, B
中科院分区：
文献类型：
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作者：
Mathiesen, T;Edner, G;Andersson, B
蛛网膜下腔出血（SAH）会引发炎症反应，并可能导致缺血性脑损伤。实验性缺血已被证明与报警反应细胞因子白细胞介素 - 1受体拮抗剂（IL - 1Ra）和肿瘤坏死因子 - α（TNF - α）有关。然而，到目前为止，在蛛网膜下腔出血事件后的患者中尚未检测到这些细胞因子水平升高。出于这个原因，我们从22名连续招募的蛛网膜下腔出血患者和10名非蛛网膜下腔出血患者（对照组）中每日采集脑脊液（CSF）样本。使用针对IL - 1Ra和TNF - α的免疫测定法对脑脊液样本进行研究，以调查蛛网膜下腔出血是否会导致细胞因子水平升高。入院时临床状况不佳的蛛网膜下腔出血患者的平均IL - 1Rα水平显著高于临床状况良好的患者（318皮克/毫升对82皮克/毫升，p < 0.02）。临床状况不佳的患者在迟发性缺血发作期间和手术后IL - 1Ra水平升高。在最终预后不良的蛛网膜下腔出血患者中，在第4天到第10天期间检测到IL - 1Ra和TNF - α显著升高（p < 0.05）。预后良好的患者和对照组患者这些细胞因子水平较低。Hunt和Hess分级为III到V级的患者手术后IL - 1Ra水平升高，但I级或II级患者则没有。这一发现表明，临床状况不佳的患者大脑处于不稳定的生化状态，这反映在手术创伤后细胞因子水平升高。已知IL - 1Ra和TNF - α都会诱发发热、不适、白细胞增多和一氧化氮合成，并介导缺血性和创伤性脑损伤。本研究表明，蛛网膜下腔出血发生后这些细胞因子水平会升高，且细胞因子高水平与脑损伤相关。因此，在蛛网膜下腔出血患者中，发热、白细胞增多和一氧化氮合成也可能由IL - 1介导，并且炎症介质可能导致脑损伤。
Subarachnoid hemorrhage (SAH) causes an inflammatory reaction and may lead to ischemic brain damage. Experimental ischemia has been shown to be connected with the alarm-reaction cytokines interleukin-1 receptor antagonist (IL-1Ra) and tumor necrosis factor-alpha (TNF alpha). Increased levels of these cytokines, however, have not been detected thus far in patients following an SAH event.For this reason daily cerebrospinal fluid (CSF) samples were collected from 22 consecutively enrolled patients with SAH and from 10 non-SAH patients (controls). The CSF samples were studied using immunoassays for IL-1Ra and TNF alpha to investigate whether an SAH caused increased cytokine levels.The mean IL-1R alpha levels were significantly higher in patients with SAH who were in poor clinical condition on admission than in those who were in good condition (318 pg/ml vs. 82 pg/ml, p < 0.02). The IL-1Ra levels increased during delayed ischemic episodes and after surgery in patients who were in poor clinical condition. Significant increases in IL-1Ra and TNF alpha were detected during Days 4 through 10 in patients suffering from SAH who eventually had a poor outcome (p < 0.05). Patients with good outcomes and control patients had low levels of these cytokines.The levels of IL-1Ra increased after surgery in patients with Hunt and Hess Grades III through V, but not in those with Grade I or II. This finding indicates that patients in poor clinical condition have a labile biochemical state in the brain that is reflected in increased cytokine levels following the surgical trauma.Both IL-1Ra and TNF alpha are known to induce fever, malaise, leukocytosis, and nitric oxide synthesis and to mediate ischemic and traumatic brain injuries. The present study shows that levels of these cytokines increase after SAH occurs and that high cytokine levels correlate with brain damage. It is therefore likely that fever, leukocytosis, and nitric oxide synthesis are also mediated by IL-l in patients suffering from SAH and it is probable that the inflammatory mediators contribute to brain damage.