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高压氧预暴露对急性氧中毒大鼠模型惊厥潜伏期影响的实验研究
引用本文:杨勐航,邵晓光,孙学军,郑娟. 高压氧预暴露对急性氧中毒大鼠模型惊厥潜伏期影响的实验研究[J]. 中华航海医学与高气压医学杂志, 2010, 17(6). DOI: 10.3760/cma.j.issn.1009-6906.2010.06.003
作者姓名:杨勐航  邵晓光  孙学军  郑娟
基金项目:第二军医大学大学生创新基金
摘    要:目的 研究高压氧预暴露对大鼠急性氧中毒潜伏期的影响并探讨其机制.方法 将40只Sprague-Dawley(SD)大鼠随机分为对照组和高压氧预暴露组,每组20只,其中高压氧预暴露组于高压纯氧(0.3 MPa)下暴露20 min,然后减至常压行空气通风20 min,如此循环4次.24 h后,将2组大鼠暴露于高压纯氧(0.5 MPa),观察40 min.检测指标包括惊厥潜伏期变化、大鼠脑组织中超氧化物歧化酶(SOD)活性和一氧化氮(NO)含量变化,进行HE染色以观察脑组织病理改变.结果 高压氧预暴露后,大鼠惊厥潜伏期[(29.79±2.13)min]比对照组[(24.25±3.76)min]延长,脑组织NO含量[(2.93±0.39)nmol/g]比对照组[(7.46±1.11)nmol/g]减少,而SOD活性与HE染色结果 显示2组差异无统计学意义.结论 高压氧预暴露可以延长大鼠惊厥潜伏期,其机制可能是高压氧降低了脑组织中的NO含量.

关 键 词:高压氧  惊厥  急性氧中毒  超氧化物歧化酶  一氧化氮

Effect of hyperbaric oxygen pretreatment on the latency of acute oxygen toxicity in rats
YANG Meng-hang,SHAO Xiao-guang,SUN Xue-jun,ZHENG Juan. Effect of hyperbaric oxygen pretreatment on the latency of acute oxygen toxicity in rats[J]. Chinese Journal of Nautical Medicine and Hyperbaric Medicine, 2010, 17(6). DOI: 10.3760/cma.j.issn.1009-6906.2010.06.003
Authors:YANG Meng-hang  SHAO Xiao-guang  SUN Xue-jun  ZHENG Juan
Abstract:Objective To investigate the effect of hyperbaric oxygen pretreatment on the latency of acute oxygen toxicity in rats and explore its mechanism. Methods Adult male SD rats were randomly divided into 2 groups: the control group and the hyperbaric oxygen pretreatment (HBOP) group. Rats in the HBOP group were exposed to pure hyperbaric oxygen for 20 min and then were decompressed to normal pressure and ventilated with air for another 20 min for a total of 4 sessions. Then, after 24 hours, the two animal groups were exposed to hyperbaric oxygen at a pressure of 0.5 MPa for 40 min. Measurement indices included changes in the latency of oxygen convulsion, activity of superoxide dismutase(SOD) and also contents of nitric oxide(NO)in the rat brain. The levels of NO and SOD in the brain tissue were also measured. HE staining was used to detect histological changes in the brain tissue. Results HBO pretreatment could significantly prolong the latency of oxygen convulsion, and also markedly reduce the content of nitric oxide(NO). SOD activity and HE staining indicated that no statistical differences could be seen in the 2 groups. Conclusions HBO pretreatment could prolong the latency of oxygen convulsion, the mechanism of which might suggest that HBO exposure could decrease the content of NO in the brain tissue.
Keywords:Hyperbaric oxygen  Convulsion  Acute oxygen toxicity  Superoxide dismutase  Nitric oxide
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