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目的探讨二氧化硫(SO2)暴露对哮喘大鼠速发相反应的影响。方法选择Wistar雄性大鼠40只,随机分为4组,每组各10只;A组为正常对照组,B组为哮喘模型组,C组为SO2低质量浓度(15 mg/m3)哮喘组,D组为SO2高质量浓度(30 mg/m3)哮喘组。每只大鼠染毒结束1周后处死,测量每只大鼠的气道阻力30 min的变化,观察肺组织病理形态学变化,采用酶联免疫吸附试验法测定血清中白细胞介素(IL)-13和IgE的水平。结果①B组大鼠的气道阻力明显高于A组,差异有统计学意义(P<0.01),C、D组大鼠的气道阻力较B组明显升高,差异有统计学意义(P<0.01);②B组大鼠血清中IL-13和IgE的水平较A组明显增高,差异有统计学意义(P<0.01),C、D组大鼠血清中IL-13和IgE的水平与B组比较差异无统计学意义(P>0.05);③肺组织病理切片实验组大鼠支气管上皮细胞部分脱落或全部脱落,大量的嗜酸性粒细胞和淋巴细胞浸润,也出现单核细胞的浸润,杯状细胞大量增生,并充填上皮细胞的位置,有大量的黏液分泌,可见黏液栓,基底膜出现纤维化。结论 SO2可加重哮喘大鼠气道高反应性和肺部变态炎症反应。
Objective To investigate the effects of sulfur dioxide (SO2) exposure on the immediate response to asthma in rats. Methods Forty Wistar male rats were randomly divided into 4 groups with 10 rats in each group. A group was normal control group, B group was asthma model group, C group was SO2 low concentration (15 mg / m3) asthma group , Group D was SO2 high concentration (30 mg / m3) asthma group. Each rat was sacrificed one week after the end of the exposure and the airway resistance of each rat was measured for 30 min. The pathological changes of the lungs were observed. The serum levels of interleukin (IL) -13 and IgE levels. Results ① The airway resistance in group B was significantly higher than that in group A, the difference was statistically significant (P <0.01). The airway resistance in group C and D was significantly higher than that in group B (P <0.01). ② The serum levels of IL-13 and IgE in group B were significantly higher than those in group A (P <0.01), while the levels of IL-13 and IgE in group C and D There was no significant difference between group B and group B (P> 0.05). ③ The bronchial epithelial cells in the experimental group were partly shedding or all falling off, a large number of eosinophils and lymphocytes infiltrated, monocyte infiltration , A large number of goblet cells hyperplasia, and filling the location of epithelial cells, a large number of mucus secretion, visible mucus plug, basement membrane fibrosis. Conclusion SO2 can aggravate airway hyperresponsiveness and lung inflammatory response in asthmatic rats.