摘要
目的:观察缺氧复合氰化钠(NaCN)中毒对大鼠心肌线粒体氧化应激反应的影响。方法:40只雄性SD大鼠随机均分为平原对照、平原中毒、高原对照、高原中毒组。高原组动物在模拟海拔4000 m的低压舱内适应3 d后开始实验。对照组动物皮下注射生理盐水。中毒组皮下注射3.6 mg/kg NaCN,分别于0.5、1、2 h时点处死动物,取心肌制备线粒体。检测线粒体羟自由基(OH.)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果:缺氧复合NaCN中毒致心肌细胞线粒体OH.、MDA含量显著升高,SOD活性显著降低。结论:相较于单纯模拟缺氧、单纯NaCN中毒,缺氧复合NaCN中毒会加重心肌线粒体的损伤。
Objective: To observe the effects of combined hypoxia and sodium cyanide (NaCN) intoxication on oxidative stress reactions in cardiac muscle mitochondfia of rats. Methods :40 male SD rats were randomly divided into plain control group,NaCN intoxicated group at 308 m altitude and high altitude control group, NaCN intoxicated group at simulated high altitude of 4000 m. Animals in two high altitude groups were scheduled to stay for 3 days in a decompression chamber till the test began. Two control groups were injected with physiological saline and intoxicated groups were injected subcutaneously with NaCN at 3.6 mg/kg. Animals were killed at 0. 5,1 and 2 hours after treatment and the mitoehondria samples were prepared from the cardiac muscle tissues. The contents of OH · and MDA as well as the SOD activity were determined by spectrephotometrie method. Results: It was demonstrated that hypoxia and NaCN injection could significantly increase the contents of OH · and MDA while decreasing the SOD activity in mitochondrial samples of rats. Conclusion: Compared with simple NaCN intoxication or simple hypobarie hypoxia, the combination of acute hypobaric hypoxia and NaCN intoxication may aggravate the cardiac muscle cytochondfiome injury.
出处
《西南国防医药》
CAS
2009年第9期861-863,共3页
Medical Journal of National Defending Forces in Southwest China
基金
全军"十一五"医药卫生科研基金资助项目(06G077)
关键词
缺氧
NaCN
心肌线粒体
氧化应激
hypobaric hypoxia
sodium cyanide
cardiac muscle eytochondriome
oxidative stress
high altitude