【摘要】 目的:观察肺气肿肺气虚证模型大鼠血液流变性变化、支气管肺泡灌洗液(BALF)中白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)含量动态变化,探讨其在肺气肿肺气虚证发病中的变化特点及其作用机制。方法:将SD大鼠随机分为对照组和模型组,每组3个时间位点(1,2,3个月),采用烟熏、气管滴入脂多糖(LPS)和饥饿等多因素复合制作肺气虚证肺气肿大鼠模型。用血液流变仪检测全血黏度、血浆黏度、红细胞比容、红细胞聚集指数、纤维蛋白原变化,采用放射免疫法检测BALF中IL10、TNFα的含量变化。结果:肺气肿肺气虚证模型大鼠动脉血全血黏度(高切、低切)、血浆黏度、红细胞比容、红细胞聚集指数及纤维蛋白原均升高,全血黏度、红细胞比容、纤维蛋白原与同时段对照组相比有显著性差异(P<0.05,P<0.01),而血浆黏度在3个月与同时段对照组相比有显著差异(P<0.05);红细胞聚集指数在2,3个月与同时段对照组相比有显著性差异(P<0.01);模型大鼠BALF中IL-10的含量降低,且3个月时最低,且与同时段对照组相比有显著性差异(P<0.01);TNF-α含量升高,且3个月时最高,与同时段对照组相比有显著性差异(P<0.05)。结论:肺气肿肺气虚证模型大鼠血液流变性降低,IL-10、TNF-α通过对免疫调节和炎性反应影响,参与肺气虚证肺气肿发病过程,且在其发病过程中起重要作用。更多还原

【Abstract】 Objective: To observe the blood rheology and contents of interleulkin-10(IL-10) and Tumor necrosis factor-α(TNFα) in bronchoalveolar lavage fluid (BALF) and investigate their roles in immunology regulation and inflammatory injury in emphysema with lung Qi-deficiency syndrome. Method: The SD rats were randomly divided into two groups:The healthy control group and model groups with the emphysema and lung Qi-deficiency syndrome which were randomly divided into three model subgroups of 1-,2-,3-month.The emphysema with lung Qi-deficiency syndrome model rats were established by intratracheal instillation of small dose of lipopolysaccharide(LPS)twice,exposure to cigarette smoking and hungry daily.The contents of IL-10 and TNFα in BALF were measured by the RIA method.At the same time,the blood rheology was observed.Result: The blood rheology decreased, the contents of IL-10 in BALF were significantly decreased in model group of 3-month compared with those of healthy control group(P<0.01),the contents of TNFα in BALF were significantly increased in model group of each month compared with those of healthy control group(P<0.05).Conclusion: The blood rheology was decreased;IL-10 and TNFα play an important role in the pathogenesis of emphysema with lung Qi-deficiency syndrome by immunoregulation and inflammatory injury.更多还原