实验性甲基汞中毒外周血液中红细胞增多及其机制的初步研究

来源 :吉林医学院学报 | 被引量 : 0次 | 上传用户:king_casper
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选用小白鼠作为主要实验动物,分为甲基汞模型组、肾切除组、对照组和假手术组。用大白鼠作为动脉血氧组。甲基汞模型组实验动物在氯化甲基汞中毒的条件下,外周血液中红细胞数量显著增多。该组动物自身红细胞数量前后对比,差异非常显著。肾切除组的实验动物,在切除一侧(左)肾脏后,发现红细胞数量均较切肾前减少。切除一侧肾脏的小白鼠,在氯化甲基汞中毒的条件下,未发现红细胞数量增多。不难看出,氯化甲基汞中毒的实验动物,其外周血液中红细胞数量增多和肾脏有极密切的关系。选用一部分大白鼠在氯化甲基汞中毒的条件下,除了外周血液中红细胞数量明显增多外,还发现该组动物的动脉血氧含量明显减少。和对照组动脉血氧含量比较,差异非常显著。由此得出结论,甲基汞中毒的小白鼠,其外周血液中红细胞数量增多的机制在于机体动脉血氧含量降低和肾脏的作用;通过肾组织缺氧导致促红细胞生成素生成增多所致。 The mice were selected as main experimental animals and divided into methylmercury model group, nephrectomy group, control group and sham operation group. Rats were used as arterial oxygen groups. Methylmercury model group experimental animals in the methylmercuric chloride poisoning conditions, the number of red blood cells in the peripheral blood increased significantly. The number of red blood cells in this group was compared before and after, and the difference was very significant. In the nephrectomized group, after removing one side (left) of the kidney, the number of red blood cells was found to be smaller than before the kidney was cut. Mice with one kidney removed were found to have an increased number of red blood cells under methylmercuric chloride poisoning conditions. It is not difficult to see that, in experimental animals poisoned with methylmercury chloride, the increase in the number of red blood cells in peripheral blood is closely related to the kidneys. In addition to the increase in the number of red blood cells in the peripheral blood, the use of a part of rats in the methylmercury chloride poisoning condition also revealed a marked decrease in the arterial blood oxygen content in this group of animals. Compared with the arterial blood oxygen content in the control group, the difference is very significant. It was concluded that the mechanism of the increase in the number of red blood cells in the peripheral blood of mice exposed to methylmercury poisoning was due to the decrease of oxygen content in the arteries of the body and the role of the kidneys, and the increase in erythropoietin production caused by hypoxia in the kidneys.
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