摘要
目的研究热应激预处理对创伤性休克早期大鼠脑组织一氧化氮(NO)浓度、诱导型一氧化氮合酶(i NOS)m RNA表达量与脑组织病理改变的影响。方法 96只SPF级雄性SD大鼠随机均分为未处理组和处理组,每组又分别设未休克组、休克后0 h、1 h、2 h、3 h及4 h组6个亚组,热应激预处理后建立创伤性休克模型,留取脑组织,观察脑组织病理学和检测脑组织NO浓度、i NOS m RNA表达量的变化。结果病理观察可见处理组各时间点脑病理损伤较未处理组病理损伤轻;NO浓度处理组均低于同时间点未处理组,休克后0 h时均有升高(P<0.05),休克后1 h时脑组织NO浓度均有明显降低(P<0.05);i NOS m RNA表达量处理组均低于同时间点未处理组,未处理组在休克后3 h出现一个峰值(3.50±0.150)u/mg·prot。结论热应激预处理能明显降低创伤性休克大鼠早期脑组织中NO、i NOS的表达,减轻创伤性休克早期大鼠脑损伤。
【Objective】 To research nitric oxide（NO） concentration, induced nitric oxide synthase（i NOS）m RNA expression and the pathological changes of brain tissue in traumatic shock rats preconditioned with heat stress. 【Methods】 A total of 96 male SD rats were randomly divided into untreated group and treatment group with equal number, and each group was equally divided into 6 subgroups： no shock group and shock 0h group, 1 h group, 2 h group, 3 h group and 4 h group. The model of traumatic shock was established after heat stress pretreatment and the brain tissue was taken for observation of pathological changes and detection of NO and i NOS m RNA expression in brain tissue. 【Results】 The lesions of brain tissue structure were lighter in the treatment group than those of the untreated group at the corresponding time point. The NO concentration of the treatment group was lower than that of the untreated group at the corresponding time point, both groups had a rise at shock 0 h（P〈0.05） and a reduce at shock 1 h（P〈0.05）. INOS m RNA expression of the treatment group was lower than that of the untreated group at the corresponding time point,there was a peak value [（3.50 ± 0.150）U/mg·prot] in the untreated group in 3 h. 【Conclusion】 Heat stress pretreatment can significantly reduce NO concentration and i NOS m RNA expression in brain tissue and alleviate the brain injury of rats in early stage of traumatic shock.
出处
《中国现代医学杂志》
CAS
北大核心
2015年第27期14-17,共4页
China Journal of Modern Medicine
关键词
热应激
创伤性休克
脑
损伤
heat stress
traumatic shock
brain
injury
