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目的:探讨严重创伤后炎性细胞凋亡与继发性坏死在急性损伤发病机制中的地位和作用。方法:复制大鼠多在骨折合并休克模型,采用Annexin—V和propidium iodide双标法经流式细胞仪检测创伤后肺泡灌洗液中凋亡与坏死炎性细胞的数量变化,测定细胞分类计数及肺通透指数并作出比较。结果:伤后动物肺泡灌洗液中巨噬细胞数量减少,而白细胞数量增加。伤后凋亡炎性细胞数量增加,于伤后3h达到高峰。部分凋亡炎性细胞继而发生继发性坏死。其数量进行性升高并与肺通透指数变化显著相关(r=0.90,p<0.01)。结论:严重创伤后肺泡灌洗液中炎性细胞发生凋亡后可能通过继发性坏死造成炎性内容物的泄漏而引发急性肺损伤。
Objective: To investigate the status and role of inflammatory cell apoptosis and secondary necrosis in the pathogenesis of acute injury after severe traumatic injury. METHODS: Most of the rats were duplicated with shock and shock model. The numbers of apoptotic and necrotic inflammatory cells in the bronchoalveolar lavage fluid were detected by flow cytometry with Annexin-V and propidium iodide double-labeled method. And pulmonary permeability index and make a comparison. Results: After injury, the number of macrophages in the alveolar lavage fluid decreased and the number of white blood cells increased. After injury, the number of apoptotic inflammatory cells increased and peaked at 3h after injury. Part of the apoptotic inflammatory cells followed by secondary necrosis. The number of patients with progressive increase and pulmonary permeability index was significantly correlated (r = 0.90, p <0.01). CONCLUSIONS: Acute lung injury may be caused by the leakage of inflammatory contents caused by secondary necrosis after apoptosis of inflammatory cells in severe post-traumatic alveolar lavage fluid.