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作 者:张伟[1] 蒋耀光[2] 谢志坚[3] 张宇[3] 胡承香[3] 李磊[3]
机构地区:[1]第三军医大学西南医院胸心外科,重庆400038 [2]第三军医大学大坪医院胸心外科,重庆400046 [3]第三军医大学大坪医院野战外科研究所,重庆400046
出 处:《重庆医学》2004年第12期1770-1772,共3页Chongqing medicine
摘 要:目的 观察严重胸部创伤后肺泡巨噬细胞免疫功能的变化 ,并探讨其意义。方法 建立严重胸部创伤模型 ,支气管肺泡灌洗分离、培养肺泡巨噬细胞 ,检测创伤前、创伤后 2、4、8、16、2 4h以及复合LPS攻击后肺泡巨噬细胞吞噬功能、抗原提呈以及细胞因子分泌等免疫功能的变化。结果 利用小型多功能生物撞击机以 4 0 0kPa驱动压力对大鼠右侧上胸壁进行致伤 ,能够建立稳定可靠并符合临床特点的严重胸部创伤模型 ;严重胸部创伤对肺泡巨噬细胞的吞噬功能表现为先增强后抑制 ;伤后其抗原提呈功能受抑 ,伤后 4h最低 ,而分泌细胞因子TNF α增强 ,伤后 4h达到高峰。结论 严重胸部创伤导致肺泡巨噬细胞免疫功能紊乱 ,本研究为创伤性急性肺损伤的发病机制提供了一定的实验及理论依据。Objective To observe the changes of immune function of alveolar macrophages. Methods A rat model of severe thoracic trauma was established, alveolar macrophages were collected by the bronchoalveolar lavage fluid,and separated and cultured. And changes of the phagocytosis, angtigen presentation and secretion of AM after trauma were observed dynamically at 2,4,8,16,24h after trauma.Results A stable and reliable severe thoracic trauma model was successfully established with 400Kpa-strike on the up-right chest of rat by a multiple-function strike apparatus. The phagocytosis of alveolar macrophages had a biphasic effects, firstly enhanced then inhibited,and its antigen-presentation was inhibited,the lowest occurred at 4h after trauma;reversely, alveolar macrophages secreted more TNF-α after trauma.Conclusion Immune function disorder was induced by severe thoracic trauma. The present study presented the valuable laboratorial and theoretical evidence for the research on ALI complicated with severe thoracic trauma.
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