Uzan M, Tanriover N, Bozkus H, Gumustas K, Guzel O, Kuday C
Department of Neurosurgery, Cerrahpasa Medical Faculty, Istanbul University, Instanbul, Turkey.
Surg Neurol. 2001 Dec;56(6):350-6. doi: 10.1016/s0090-3019(01)00633-4.
This article investigates nitric oxide (NO) metabolism following severe head injury (SHI). We wished to clarify the alterations of NO metabolism end products that is associated with SHI, and to delineate the role of inflammation in this process.
In a prospective study, we simultaneously measured the concentrations of NO metabolites and interleukin-8 (IL-8) in the ventricular cerebrospinal fluid (CSF) of 11 patients who had suffered SHI. The CSF concentrations of nitrite (NO(-)(2)) and nitrate (NO(-)(3)) combined, and of IL-8 were measured during the following four time periods post-trauma: 6 to 10, 20 to 28, 40 to 56, and 64 to 74 hours. Levels were measured using the corresponding kits.
Compared to the ventricular CSF control values, all of our SHI patients had significantly elevated CSF levels of NO(-)(2) plus NO(-)(3) (NO(-)(2) + NO(-)(3)) and IL-8 during all periods tested. CSF NO(-)(2) + NO(-)(3) and IL-8 concentrations reached their maximums simultaneously at 20 to 28 hours following trauma (Spearman's rank correlation = 0.609, p < 0.05), and NO(-)(2) + NO(-)(3) levels were significantly higher than those measured at 6 to 10, 40 to 56, and 64 to 74 hours. [Nitrite-nitrate concentrations: 6-10 hours: 19.22 +/- 6.75, 20-28 hours: 25 +/- 6.2 micromol/l, 40-56 hours: 19.82 +/- 4.47, and 64-74 hours: 19.72 +/- 4.61 micromol/l, (p < 0.05). IL-8 concentrations: 6-10 hours: 3,232 +/- 2,976.2, 20-28 hours: 3,458.45 +/- 3,048 pg/mL, 40-56 hours: 2,616.41 +/- 2,539.21, 64-74 hours: 1,388.88 +/- 1,216.7 pg/mL, (p < 0.001).]. This simultaneous surge in NO(-)(2) + NO(-)(3) and IL-8 in the initial 24 hours post-traumatic indicated that inflammation secondary to SHI increased the rate of NO metabolism, resulting in higher levels of metabolites in the CSF.
In patients with SHI, CSF concentrations of the dominant metabolites of NO are elevated in the first 3 days after trauma. A similar concurrent spike in the CSF level of IL-8, a marker of acute inflammatory response, can also be demonstrated. These data indicate that the predominant cause of the higher CSF NO(-)(2) + NO(-)(3) concentrations observed in SHI is most likely inflammation.
本文研究重度颅脑损伤（SHI）后的一氧化氮（NO）代谢情况。我们希望阐明与SHI相关的NO代谢终产物的变化，并明确炎症在此过程中的作用。
在一项前瞻性研究中，我们同时测量了11例SHI患者脑室脑脊液（CSF）中NO代谢产物和白细胞介素-8（IL-8）的浓度。在创伤后的以下四个时间段测量亚硝酸盐（NO₂⁻）和硝酸盐（NO₃⁻）的合并CSF浓度以及IL-8浓度：6至10小时、20至28小时、40至56小时和64至74小时。使用相应试剂盒测量水平。
与脑室CSF对照值相比，所有SHI患者在所有测试时间段内CSF中NO₂⁻加NO₃⁻（NO₂⁻ + NO₃⁻）和IL-8水平均显著升高。CSF中NO₂⁻ + NO₃⁻和IL-8浓度在创伤后20至28小时同时达到最大值（Spearman等级相关性 = 0.609，p < 0.05），且NO₂⁻ + NO₃⁻水平显著高于在6至10小时、40至56小时和64至74小时测量的值。[亚硝酸盐 - 硝酸盐浓度：6 - 10小时：19.22 ± 6.75，20 - 28小时：25 ± 6.2微摩尔/升，40 - 56小时：19.82 ± 4.47，64 - 74小时：19.72 ± 4.61微摩尔/升，（p < 0.05）。IL-8浓度：6 - 10小时：3232 ± 2976.2，20 - 28小时：3458.45 ± 3048皮克/毫升，40 - 56小时：2616.41 ± 2539.21，64 - 74小时：1388.88 ± 1216.7皮克/毫升，（p < 0.001）。]创伤后最初24小时内NO₂⁻ + NO₃⁻和IL-8的同时激增表明，SHI继发的炎症增加了NO代谢速率，导致CSF中代谢产物水平升高。
在SHI患者中，创伤后前3天CSF中NO的主要代谢产物浓度升高。同时，作为急性炎症反应标志物的CSF中IL-8水平也会出现类似的同步峰值。这些数据表明，在SHI中观察到的CSF中较高的NO₂⁻ + NO₃⁻浓度的主要原因很可能是炎症。
