Magnesium and the inflammatory response: potential pathophysiological implications in the management of patients with aneurysmal subarachnoid hemorrhage?
Magnesium and the inflammatory response: potential pathophysiological implications in the management of patients with aneurysmal subarachnoid hemorrhage?
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DOI：
10.1684/mrh.2012.0314
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发表时间：
2012-07-01
影响因子：
3.2
通讯作者：
Keller, Emanuela
中科院分区：
文献类型：
--
作者：
Muroi, Carl;Burkhardt, Jan-Karl;Keller, Emanuela
动脉瘤性蛛网膜下腔出血（SAH）患者的脑血管痉挛和迟发性脑缺血仍然是一个尚未解决的问题。理论上，高剂量硫酸镁 (MgSO4) 疗法具有血管和神经保护作用，因此目前正在评估中。 SAH 后炎症反应的强度与结果相关。本研究的目的是评估炎症反应与 MgSO4 治疗之间可能存在的联系，因为镁 (Mg2+) 具有抗炎特性。在 15 名 SAH 患者中，第 4 天至第 12 天期间，每天使用酶联免疫吸附测定法测定脑脊液 (CSF) 和外周血中的炎症细胞因子水平。8 名患者仅接受标准治疗（第 1 组），7 名患者接受额外的高剂量 MgSO4 治疗（第 2 组）。第 2 组的血清 Mg2+ 水平显着高于第 1 组：1.48 +/- 0.04 mmol/L 对比 0.90 +/- 0.01 mmol/L，rho < 0.001。与第 1 组相比，第 2 组脑脊液中的白介素 6 (IL-6) 显着降低：6680 +/- 989 vs. 11079 +/- 1277 pg/mL，rho = 0.021。第 2 组中发现全身 IL-6 水平较低的趋势：58 +/- 7 与 104 +/- 21 pg/mL，rho = 0.052。第 2 组的全身 IL-1 β 水平显着较低：0.66 +/- 0.11 和 0.15 +/- 0.01 pg/mL (rho < 0.001)，而脑脊液水平没有差异。两组之间的肿瘤坏死因子-α水平没有差异。虽然第2组有更多患者获得良好的结果，但差异无统计学意义。这可能是由于样本量较小。结果表明，在接受高剂量 MgSO4 治疗的患者中，炎症细胞因子的释放受到抑制，特别是 IL-6。这些结果需要进一步研究 Mg2+ 对 SAH 后迟发性脑缺血炎症信号通路的影响。
Cerebral vasospasm and delayed cerebral ischemia remain an unsolved problem in patients with aneurysmal subarachnoid hemorrhage (SAH). In theory, high-dose magnesium sulfate (MgSO4) therapy offers vascular and neuroprotective benefits and is therefore currently under evaluation. The intensity of the inflammatory response after SAH is associated with the outcome. The aim of the current study was to evaluate a possible link between the inflammatory response and MgSO4 therapy, since magnesium (Mg2+) has anti-inflammatory properties. In 15 patients with SAH, inflammatory cytokine levels in the cerebrospinal fluid (CSF) and peripheral blood were determined daily using an enzyme-linked immunosorbent assay between day 4 and day 12. Eight patients were treated with standard therapy alone (group 1) and seven patients were treated with an additional, high-dose of MgSO4 (group 2). Serum Mg2+ levels in group 2 were significantly higher compared to group 1: 1.48 +/- 0.04 mmol/L versus 0.90 +/- 0.01 mmol/L, rho < 0.001. Interleukin-6 (IL-6) in the CSF was significantly lower in group 2 compared to group 1: 6680 +/- 989 vs. 11079 +/- 1277 pg/mL, rho = 0.021. A trend towards lower systemic IL-6 levels was found in group 2: 58 +/- 7 versus 104 +/- 21 pg/mL, rho = 0.052. Systemic IL-1 beta levels were significantly lower in group 2: 0.66 +/- 0.11 and 0.15 +/- 0.01 pg/mL (rho < 0.001), while the CSF levels did not differ. Tumor necrosis factor-alpha levels did not differ between the two groups. Although there were more patients with favorable outcome in group 2, the difference was not statistically significant. This was probably due to the small sample size. The results indicate a suppression of inflammatory cytokine release, in particular IL-6, in patients treated with high-dose MgSO4. These results call for further studies of the effect of Mg2+ on the inflammatory signaling pathway with regard to delayed cerebral ischemia following SAH.