论文部分内容阅读
硫化物中毒(H_2s吸入或Na_2S注入)的机制,通常认为是抑制细胞色素氧化酶,与氰化物中毒相似。中毒时组织中氧的利用率降低,结果血氧张力高于正常,故在血液输氧功能受损以前,给氧是不必要的。但在急性硫化物中毒时,给氧被广泛认为是首选的解毒剂。对氰化物急性中毒的小鼠给氧、硫代硫酸盐及亚硝酸盐合用比不用氧时效果更好些。本实验观察在硫化物中毒时是否也有此效果。用雄性小鼠(25～30g)进行二种实验。第一种实验给小鼠注射一定剂量的硫化钠使中毒,在注前分别给硫代硫酸钠、亚硝酸钠、及二者合用等各种预处理,对照组不给任何预处理。每种预处理组及对照组均
Sulfide poisoning (H 2 s inhalation or Na 2 S injection) mechanism, usually considered to be cytochrome oxidase, is similar to cyanide poisoning. Oxygen utilization in tissues is reduced as a result of poisoning, and as a result blood oxygen tension is higher than normal, oxygen administration is not necessary until the oxygen transport function of the blood is impaired. However, in acute sulfide poisoning, oxygen is widely considered as the preferred antidote. Acute toxicity of cyanide in mice oxygen, thiosulfate and nitrite than the effect of oxygen better. This experiment observed whether this effect is also caused by sulfide poisoning. Two experiments were performed with male mice (25-30g). In the first experiment, mice were injected with a dose of sodium sulfide for poisoning. Before the injection, sodium thiosulfate, sodium nitrite and the combination of the two were separately pretreated. The control group did not give any pretreatment. Each pretreatment group and control group were