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作 者:桂平[1] 武庆平[1] 姚尚龙[1] 李建蓉[2] 李永平[2]
机构地区:[1]华中科技大学同济医学院附属协和医院麻醉科,武汉市430022 [2]华中科技大学同济医学院病原生物系,武汉市430022
出 处:《中华麻醉学杂志》2009年第4期308-310,共3页Chinese Journal of Anesthesiology
基 金:基金项目:国家自然科学基金资助项目(30571787)
摘 要:目的观察呼吸机相关性肺炎大鼠肺组织β-防御素-3(BD-3)的表达,探讨呼吸机相关性肺炎的发病机制。方法清洁级雄性SD大鼠20只,体重240~290g,随机分为2组(n=10):非呼吸机相关性肺炎组(N组)和呼吸机相关性肺炎组(V组)。两组均经口气管插管,N组气管内注入10^10 cfu/ml耐甲氧西林金黄色葡萄球菌菌液0.2ml;V组机械通气4h时气管内注入等容量耐甲氧西林金黄色葡萄球菌菌液,注入菌液后拔出气管导管。于注入菌液后48h时处死大鼠,取肺组织,计算肺湿重占体重百分比,行秭组织肉眼下和镜下的病理学评分,测定肺组织细菌计数,记录菌血症的发生情况,免疫组化法测定肺组织BD-3的表达水平。结果与N组比较,V组肺湿重占体重百分比、肺组织镜下病理学评分、肺组织细菌计数和菌血症发生率升高,肺组织BD-3表达下调(P〈0.01)。结论大鼠呼吸机相关性肺炎的发病机制与肺组织BD-3的表达下调有关。Objective To investigate the role of beta-defensin-3 (BD-3) in lung tissue in a rat model of ventilator-associated pneumonia. Methods Twenty pathogen-free male SD rats weighing 240-290 g were randomly divided into 2 groups (n = 10 each): non-ventilator-associated pneumonia group (group N) and wentilatorassociated pneumonia group (group V). The animals were anesthetized with intraperitoneal (IP) 20% urethane 1.3 g/kg. Oral tracheal intubation was performed under direct vision. In group N the animals kept spontaneous breathing. MRSA suspension (10^10 cfa/ml) 0.2 ml was introduced into bronchus immediately after tracheal intubation. The animals were then extubated. In group V the animals were mechanically ventilated (VT 6 ml/kg, RR 88 bpm, PEEP 5 cm H2 O, FiO2 21% ) for 4 h. MRSA suspension (10^10 cfu/ml) 0.2 ml was introduced into bronchus at the end of 4 h mechanical ventilation. The animals were killed at 48 h after inoculation in both groups. The lungs were removed for microscopic examination of pathologic changes which were scored. Wet lung weight/body weight ratio (WW/BW) was measured. Lung bacterial counts and spleen culture were performed. The expression of BD-3 in lung tissue was detected by immuno-histochcmical staining. Results WW/BW, lung pathology scores, lung bacterial counts and the incidence of bacteremia were significantly higher in group V than in group N, while BD-3 expression in lung tissue was significantly lower in group V than in group N. Conclusion The pathogencsis of ventilator-associated pneumonia is related to the down-regulation of BD-3 expression in rat lung tissue.
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