摘要
目的观察不安全减压后制成的减压病模型大鼠体内炎症因子的改变。方法以雄性SD大鼠为实验动物制成减压病模型,用压缩空气在3 min内匀速加压至0.7 MPa,停留60 min后在3 min内快速减压出舱。分别在减压后0.5、6、24h取大鼠肺、肝、脑组织,甲醛溶液固定,石蜡包埋,切片,HE染色后观察其病理变化。分别在减压后0.5、6、24 h,从大鼠球后静脉丛取血,ELISA测定血清中炎症因子IFN-γ、TNF-α及IL-6的表达。结果大鼠肺、肝及脑组织在不安全减压后出现水肿、淤血等病理表现,以减压后0.5 h内最为显著。和正常对照组相比,减压病模型大鼠血清IFN-γ,TNF-α及IL-6含量显著上升。结论炎症因子表达增高是减压病致机体组织损伤加重的因素之一。
Objective To observe the changes of inflammatory mediators in rat models which were made by unsafe decompression. Methods The male SD rats were selected for laboratory animals be made into decompression models. The laboratory rats were placed in the hyperbaric chamber. The air in the chamber was compressed to 0.7 MPa within 3 minutes and held at the designated depth for 60 min, then rapidly （within 3 min） decompressed to the surface. At 30 min, 6 or 24 h after decompression, the rats were killed and their brain, livers, and lungs were taken out of and fixed before dehydration and embedding in paraffin. Sections were placed on glass slides and stained with hematoxylin and eosin for routine histologic analysis. At 30 min, 6 or 24 h after decompression, serum samples of rats were collected via post-global veins and analyzed by ELISA for TNF-α, IL-6, and IFN-γ. Results Pathological changes including oedema and congestion in the lungs, liver and brain were found after unsafe decompression, especially within 30 rain after decompression. Compared with the normal rats, the levels of IFN-γ, TNF-α and IL-6 in the serum samples of decompression sickness rats significantly increased. Conclusion The high expression of inflammatory mediators is one of the factors which may induce that decompression sickness make tissue damage aggravate.
出处
《海军医学杂志》
2010年第4期291-292,323,共3页
Journal of Navy Medicine
基金
海军后勤部基金项目(07-3301)
