烟雾吸入伤动物模型的建立及评价

doi:10.3969/j.issn.1002-1949.2018.06.018

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摘要目的建立烟雾吸入伤大鼠模型，探讨大鼠致伤后体内病理生理及炎症因子变化。方法将42只雄性Wistar大鼠随机分为七组：正常对照组（n=6），烟雾吸入性损伤组，该组分为S1、S2、S3、S7、S14、S28六个亚组（n=36），分别于致伤后1、2、3、7、14、28 d（每组n=6）取材，肺组织HE染色观察烟熏造模后相应时间点病理学改变；检测肺组织湿干质量比评价肺水肿程度；ELISA检测血浆及支气管肺泡灌洗液中白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的含量。结果肺组织病理学显示，致伤前3 d为发病急性期，以大气道周围病变为主，气道上皮细胞纤毛结构破坏，气道内局部分泌物增加，同时伴有局部肺泡间质增厚、破裂融合；致伤7 d后主要表现为局部肺间质病变，肺泡融合，偶见炎性细胞侵润灶；致伤28 d大部分出现大片状间质病变，局部肺部纤维化表现。S1、S2组大鼠肺湿干质量比高于正常对照组（P=0.001，P=0.014），损伤S7、S14、S28组明显低于损伤S1组（P=0.018，P=0.024，P=0.014）。与正常对照组比较，大鼠血浆IL-6在损伤后未见明显改变；肺泡灌洗液中IL-6损伤后未出现明显改变，于损伤28 d后出现轻度降低（P＜0.05）；大鼠损伤1 d后血浆中TNF-α含量出现明显升高，而损伤S28组血浆TNF-α含量明显低于正常对照组（P＜0.05），肺泡灌洗液中TNF-α含量损伤后明显升高，于损伤后2 d和14 d出现两个高峰（P＜0.05）。结论烟雾吸入后病理损伤及炎症因子改变呈现一定规律，本研究为阐明烟雾吸入伤的发病机制及救治研究提供了实验依据和策略。

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	肖培欣
	孙淑丽
	王敬
	李和林
	丁辉
	白松
	刘子泉
	曹娟
	刘晋阳
	王雪
	吕琪
	樊毫军

关键词 ：烟雾吸入性损伤, 大鼠, 炎症因子, 白细胞介素-6（IL-6）, 肿瘤坏死因子-α（TNF-α）

通讯作者: 樊毫军（1974-），男，博士，主任医师，硕士生导师，武警后勤学院附属医院救援医学研究所副所长，E-mail:fanhaojun999@126.com；吕琪（1984-），男，博士，天津大学灾难医学研究院副教授，E-mail:lvqi68@163.com。

作者简介: 肖培欣（1992-），女，硕士研究生，E-mail:360152518@qq.com。

引用本文:

肖培欣，孙淑丽，王敬，李和林，丁辉，白松，刘子泉，曹娟，刘晋阳，王雪，吕琪，樊毫军. 烟雾吸入伤动物模型的建立及评价[J]. 中国急救医学, 2018, 38(6): 543-.
Xiao Pei-xin, Sun Shu-li, Wang Jing, Li He-lin, Ding Hui, Bai Song, Liu Zi-quan, Cao Juan, Liu Jin-yang, Wang Xue, Lv Qi, Fan Hao-jun. Establishment and evaluation of animal model of smoke inhalation injury. Chinese Journal of Critical Care Medicine, 2018, 38(6): 543-.

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http://www.cnemergency.org.cn/CN/10.3969/j.issn.1002-1949.2018.06.018 或 http://www.cnemergency.org.cn/CN/Y2018/V38/I6/543

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