大鼠实验性急性氰化物中毒时脑组织的病理变化及其发生机制的研究

Experimental Study on Pathological Changes and Their Mechanism in Rat Brain Tissue with Acute Cyanide Poisoning

本文结合血液、脑组织CN^-浓度测定和脑组织细胞色素氧化酶活性定量分析,对大鼠急性NaCN中毒(4.5mg/kg i.p.)后21h内脑组织的病理变化进行了动态观察,结果表明:大鼠腹腔注射低于致死剂量的NaCN(80％LD)造成急性中毒后,脑组织可出现明显的病理变化,以细胞色素氧化酶低活性分布区为重。其基本病理变化为:(1)神经细胞、神经胶质细胞变性、坏死;(2)各种细胞突起成份变性、肿胀、溶解;(3)有髓神经纤维髓鞘破坏。这些病理变化的产生和发展。表现为一动态过程,大致可分为3个时期:(1)代谢紊乱期;(2)损伤反应期;(3)恢复期。本文认为,动物急性中毒反应的发生,是NaCN注射后脑组织细胞色素氧化酶活性受到强烈抑制的直接结果;随后出现的震颤、不稳、共济失调等则可能与继发的脑组织结构损伤有关。本文还对氰化物中毒后脑组织病理变化产生的机制进行了讨论。

Observations on the developement of pathological changes of rat brain, together with dynamic detection of CN- concentrations in blood and brain tissue and quantitive analysis of brain cytochrome oxidase activity, are carried out within 24 h after acute cyanide intoxication (4.5mg/kg i.p.) . The results indicate that in the cyanide poisoning with the dose under lethality (80%LD) , the pathological changes in rat brain appear, especially in cytochrome oxidase poorly- contained areas, including! 1 ) degeneration and necrosis of neurons and gliocytes; 2) degeneration, swelling and lysis of different cell projection components; 3) the myelinoclasis of myelinated nerve fibers. Those changes undergo a dynamic course divided into three phases: 1 ) the phase of metabolic disturbance; 2) of response to injury; and 3) of restoration. The authors consider that the acute poisoning displayed by the animal after NACN injection is directly caused by the intense inhibation of brain cytochrome oxidase; the secondary lesions of brain structure may be responsible for the manifestations such as trembling, unstable, and ataxia etc.occur later. The mechanisms of the brain pathological changes after cyanide intoxication are also disscussed.