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目的分析慢性汞中毒患者脑脊液汞含量的变化,探讨汞的神经毒性机制。方法选择9例慢性汞中毒患者作为中毒组,8例非汞接触患者为对照组,用碱性氯化亚锡还原-冷原子吸收光谱法测定24 h尿汞(U-Hg)和脑脊液汞(CSF-Hg)含量,用酸陸氯化亚锡还原-冷原子吸收光谱法测定同一天的血汞(B-Hg)含量；5例慢性汞中毒患者作驱汞前后B-Hg、U-Hg和CSF-Hg含量比较。结果中毒组B-Hg、U-Hg含量[(250．00±48．54)、(160．07±91．15)nmol/L]均明显高于对照组[(81．04±63．01)、(24．73±9．96)nmol/L],差异有统计学意义(P＜0．01)；中毒组CSF-Hg含量为(20．22±10．21) nmol/L,对照组CSF-Hg未检出。5例慢性汞中毒患者用二巯丙磺酸钠作2～3疗程驱汞治疗,B-Hg、U- HC、CSF-Hg含量治疗前分别为(258．00±48．68)、(141．02±63．74)和(22．60±7．14)nmol/L,治疗后明显下降,分别为(172．00±68．34)、(39．22±11．83)和(11．32±4．92)nmol/L,差异有统计学意义(P＜0．05或P＜0．01)。中毒组CSF-Hg含量与B-Hg含量有相关关系(P＜0．05),与U-Hg含量无相关关系(P＞0．05),但驱汞治疗后,CSF-Hg含量的下降与B-Hg、U-Hg含量下降的相关性均无统计。结论慢性汞中毒患者CSF-Hg含量随外周血汞升高而升高,但与U-Hg含量无关；而驱汞治疗后,B-Hg、U-Hg含量已正常,但CSF-Hg含量仍较高,其可能为引起慢性汞中毒患者神经行为功能改变和震颤等临床表现的基础物质。
Objective To analyze the changes of cerebrospinal fluid mercury in patients with chronic mercury poisoning and to explore the mechanism of mercury toxicity. Methods Nine patients with chronic mercury poisoning were selected as poisoning group and eight patients without mercury exposure as control group. Mercury 24 h (U-Hg) and cerebrospinal fluid mercury (Hg) were determined by alkaline stannous chloride reduction-cold atomic absorption spectrometry CSF-Hg). The content of blood mercury (B-Hg) on the same day was detected by acid-base stannous chloride reduction-cold atomic absorption spectrometry. The levels of B-Hg, U-Hg And CSF-Hg content comparison. Results The contents of B-Hg and U-Hg in the poisoning group were significantly higher than those in the control group [(250.00 ± 48.54), (160.07 ± 91.15) nmol / L [(81.04 ± 63.01 (24.73 ± 9.96) nmol / L], the difference was statistically significant (P <0.01). The content of CSF-Hg in the poisoning group was (20.22 ± 10.21) nmol / L, Group CSF-Hg was not detected. Five patients with chronic mercury poisoning were treated with mercaptosuccinate for 2 ~ 3 courses, and the levels of B-Hg, U-HC and CSF-Hg were 258.00 ± 48.68 and 141 respectively .02 ± 63.74) and (22.60 ± 7.14) nmol / L, respectively, and decreased significantly after treatment (172.00 ± 68.34, 39.22 ± 11.83, and .32 ± 4.92) nmol / L, the difference was statistically significant (P <0.05 or P <0.01). The content of CSF-Hg in the poisoning group was correlated with the content of B-Hg (P <0.05), but not with the content of U-Hg (P> 0.05) And B-Hg, U-Hg decreased correlation was no statistics. Conclusions CSF-Hg levels in patients with chronic mercury poisoning increased with the increase of peripheral blood mercury, but not with the content of U-Hg. After excretion of mercury, B-Hg and U-Hg contents were normal, but CSF-Hg content Higher, which may be caused by chronic mercury poisoning in patients with neurobehavioral changes and tremor and other clinical manifestations of the basic material.