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目的:建立大鼠COPD急性加重期模型的方法,确定滴注感染细菌的浓度。方法:雄性Wistar大鼠随机分为对照组、模型组(每组再分为高、中、低细菌浓度组,空白组)。进行一般体征的观察,基础体温的测定,感染前后血清中白细胞总数测定,肺组织病理形态的观察。结果:从对照组及COPD模型组的基础体温测定看,高浓度细菌组的基础体温高于中、低浓度组及空白组。对照组:高浓度细菌组的白细胞计数均高于对照组中、低浓度组及空白组(t=-4.012,P<0.05;t=-3.939,P<0.05;t=-6.52,P<0.01);模型组:低、中、高浓度组WBC计数高于空白组(t=-4.517,P<0.05;t=-10.32,P<0.01;t=-7.094,P<0.01);高、中浓度组WBC计数高于低浓度组(t=-4.32,P<0.05;t=-3.86,P<0.05)。并且无论是对照组还是模型组,高浓度细菌组感染后白细胞计数明显高于感染前白细胞计数(t=-14.319,t=-7.06,P<0.01)。从病理学角度看,对照组的高浓度细菌组的肺组织病理学改变符合人类肺炎的病理表现,COPD模型组的高浓度细菌组的肺组织病理学改变符合人类COPD合并肺炎的病理表现。结论:用熏吸香烟加气管内注射内毒素及鼻腔反复高浓度滴入金黄色葡萄菌(细菌浓度为2.4×109cfu/mL)的方法可建立大鼠AECOPD模型,可用于实验研究。
Objective: To establish a method for acute exacerbation of chronic obstructive pulmonary disease (COPD) in rats and to determine the concentration of bacteria instilled infection. Methods: Male Wistar rats were randomly divided into control group and model group (each group was divided into high, medium and low bacterial concentration group, blank group). The general signs of observation, the determination of basal body temperature, the determination of the total number of leukocytes in the serum before and after infection, lung histopathology observation. Results: The basal body temperature of the control group and COPD model group was higher than that of the medium and low concentration groups and the blank group. In the control group, the leukocyte counts in the high-concentration bacteria group were higher than those in the control group, the low-concentration group and the blank group (t = -4.012, P <0.05; t = -3.939, P < ); Model group: WBC count in low, middle and high concentration group was higher than that in blank group (t = -4.517, P <0.05; t = -10.32, P <0.01; t = -7.094, P <0.01) The concentration of WBC was higher than the low concentration group (t = -4.32, P <0.05; t = -3.86, P <0.05). And in both control and model groups, the leukocyte counts in high-concentration bacteria group were significantly higher than those before infection (t = -14.319, t = -7.06, P <0.01). From the pathological point of view, the pathological changes of the lung tissue of the high-concentration bacteria group in the control group were in accordance with the pathological findings of the human pneumonia. The pathological changes in the high-concentration bacteria group in the COPD model group were in line with the pathological findings of human COPD-associated pneumonia. Conclusion: The AECOPD model of rats can be established by injecting endotoxin with smoked cigarettes and repeated high concentration of nasal instillation of S. aureus (bacterial concentration of 2.4 × 109 cfu / mL), which can be used in experimental study.