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首页> 外文期刊>Undersea and Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society >Effect of acute and delayed hyperbaric oxygen therapy on cyanide whole blood levels during acute cyanide intoxication.
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Effect of acute and delayed hyperbaric oxygen therapy on cyanide whole blood levels during acute cyanide intoxication.

机译:急性和延迟高压氧的效果治疗氰化物在全血水平急性氰化物中毒。

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摘要

Cyanide and carbon monoxide, which are often found in fire victims, are toxic gases emitted from fires. Cyanide and carbon monoxide have similar molecular structure. Cyanide binds to the enzyme cytochrome oxidase a, a3 similar to carbon monoxide, thus blocking the mitochondrial respiration chain causing depletion of adenosine triphosphate. Hyperbaric oxygen (HBO2) is recommended for treating carbon monoxide poisoning. The therapeutic effect is due to a high oxygen pressure removing carbon monoxide from the cells. We hypothesise that HBO2 induces changes in whole-blood-cyanide by a competitive mechanism forcing cyanide out of cellular tissues. A rat model was developed to study this effect. Female Sprague Dawley rats were anesthetized with a fentanyl + fluanizone combination and midazolam given subcutaneously (s.c.). Rats were poisoned with 5.4 mg/kg KCN injected intra-peritoneally in Group 1 and intra-arterially in Group 2. Blood samples were taken immediately after poisoning, and at one and a half, three and five hours. Blood was drawn from a jugular vein in Group 1 and from a femoral artery in Group 2. Group 1 rats were divided into a control group of 12 rats without HBO2, 10 rats had acute HBO2 immediately after poisoning and a group of 10 rats had HBO2 one and a half hours after poisoning. Group 2 rats were divided into a control group and an acute HBO2 group, with 10 rats in both groups. Whole-blood-cyanide concentrations were measured using the Conway method based on diffusion and the subsequent formation of cyanocobalamin measured by a spectrophotometer. Results showed that whole-blood-cyanide concentration in Group 1 controls and acute HBO2 initially rose and then fell towards zero. In rats treated with delayed HBO2, the reduction in whole-blood-cyanide concentration was significantly less as compared to controls and acute HBO2-treated rats. Group 2 controls whole-blood-cyanide concentration decreased towards zero throughout the observation period. However, in Group 2 acute HBO2-treated rats a secondary rise in whole-blood-cyanide was observed. The study indicates that HBO2 can move cyanide from tissue to blood. These findings may be of clinical importance, as combined HBO2 and antidote treatment, may accelerate detoxification.
机译:氰化物和一氧化碳,常常发现在火灾受害者,有毒气体排放火灾。分子结构。细胞色素氧化酶,a3类似于碳一氧化碳,从而阻止线粒体腺苷的呼吸链造成损耗三磷酸腺苷。推荐治疗一氧化碳中毒。高氧压力去除一氧化碳从细胞。改变whole-blood-cyanide竞争细胞机制迫使氰化物组织。的效果。芬太尼+ fluanizone麻醉组合和咪达唑仑皮下注射(南)。注射intra-peritoneally组1和在2组动脉内的。后立即中毒,和半,三到五小时。从一个在组1和股骨颈静脉动脉组2。12的对照组老鼠没有HBO2, 10大鼠急性中毒后立刻HBO2,10组老鼠HBO2一个半小时后中毒。对照组和急性HBO2集团10在两组大鼠。使用康威浓度测定基于扩散和随后的方法维生素b12测量的形成分光光度计。在组1 whole-blood-cyanide浓度控制和急性HBO2最初上涨下降为零。HBO2 whole-blood-cyanide减少浓度相比明显减少控制和急性HBO2-treated老鼠。控制whole-blood-cyanide浓度整个观察下降为零时期。老鼠whole-blood-cyanide二次上升观察到。氰化物从组织到血液。结合HBO2和临床的重要性解药治疗,可能会加速解毒。

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