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目的 全氟异丁烯 (PFIB)是一种具有强大肺杀伤作用、可穿透防毒面具的潜在性化学战剂。其毒性作用机制目前尚未完全阐明。本研究拟就肺泡巨噬细胞 (AM)在PFIB急性吸入性肺损伤中的作用进行初步探讨。方法 雄性昆明小鼠 ,随机分为 4组 ,即对照组、氯化钆 (GdCl3)组、PFIB组和GdCl3/PFIB组。其中PFIB和GdCl3/PFIB组分别在中毒前4 8h及 2 4h各尾静脉iv 10mg·kg- 1GdCl31次 ,对照与PFIB组给予等剂量生理盐水。之后对照组与GdCl3组进行过滤空气暴露 ,PFIB组与GdCl3/PFIB组进行全身暴露PFIB中毒 ,PFIB中毒剂量为 130mg·m- 3× 5min。分别在中毒结束后 8,12 ,2 4 ,4 8和72h ,测定支气管肺泡灌洗液 (BALF)中总蛋白含量及肺组织湿 /干重比 ;在中毒结束后 2 4h观察组织及超微病理改变 ;并观察在 190mg·m- 3× 5min中毒剂量下小鼠 7d内的死亡率。结果 预先抑制AM功能可显著降低PFIB中毒小鼠死亡率 (P <0 .0 5 ) ,改善PFIB所致的肺组织及超微病理改变 ;在中毒后 8,12 ,2 4h ,可显著降低BALF中总蛋白含量(与相应时间点的PFIB组比较 ,P <0 .0 5 ) ,明显降低肺湿 /干重比 (其中 8,2 4h与相应时间点的PFIB组比较 ,P <0 .0 1;12h与PFIB组比较 ,P <0 .0 5 )。以上各时点的BALF中总蛋白含量与正常对照组比较显著升高
Objective Perfluoroisobutylene (PFIB) is a potential chemical warfare agent that can penetrate gas masks with strong lung-killing effect. The mechanism of its toxicity has not yet been fully elucidated. This study was to investigate the role of alveolar macrophages (AMs) in acute lung injury induced by PFIB. Methods Male Kunming mice were randomly divided into 4 groups: control group, gadolinium chloride (GdCl3) group, PFIB group and GdCl3 / PFIB group. The PFIB and GdCl3 / PFIB groups were iv iv at 10 mg · kg-1 GdCl for 48 h and 48 h before poisoning, respectively. The control and PFIB groups were given equal doses of normal saline. Afterwards, the control group and the GdCl3 group were subjected to filtered air exposure. The PFIB group and the GdCl3 / PFIB group were subjected to whole-body exposure PFIB poisoning at a dose of 130 mg · m-3 × 5 min. The total protein and the ratio of wet to dry weight of lung in bronchoalveolar lavage fluid (BALF) were measured at 8, 12, 24, 48 and 72 h after poisoning respectively. The tissue and ultrastructure were observed 24 h after the poisoning Pathological changes; and observed in 190mg · m-3 × 5min toxic dose within 7d mortality in mice. Results Pretreatment of AM function could significantly reduce the mortality of PFIB-poisoned mice (P <0.05), and improve the pathological changes of lung tissue and ultrastructure induced by PFIB. At 8, 12 and 24 hours after poisoning, BALF (P <0.05), and significantly decreased the lung wet / dry weight ratio (8,2 4 h, P <0. 0 compared with the PFIB group at the corresponding time point 1; 12h compared with PFIB group, P <0.05). The total protein in BALF at all time points was significantly higher than that in the normal control group