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目的:探讨急性呼吸窘迫综合征 (ARDS)过程所继发的肺外器官损伤中小肠组织脂质过氧化和一氧化氮 (NO)的动态变化及其作用。方法:用油酸诱发兔 ARDS模型 ,并分为 30、6 0、90和 12 0 m in4组 ,测量每组小肠组织谷胱甘肽过氧化物酶 (GPH- Px)、丙二醛 (MDA)及 NO的含量。 结果 :(1)油酸各时间组小肠组织 GPH- Px、MDA含量与对照组相比差异有统计学意义 (P<0 .0 5～ 0 .0 1) ,而且两者呈负相关 (r=- 0 .98,P<0 .0 1)。 (2 )小肠组织 NO含量油酸 30 m in组比对照组明显增加 (P<0 .0 1) ,而在油酸 6 0 m in以后各组与油酸 30 min组相比又有所减少 (P均 <0 .0 1)。结论:油酸致 ARDS过程中 ,自由基产生增多 ,诱发脂质过氧化 ,使 NO生成增多 ,机体各脏器功能损伤 ,尤其降低胃肠道屏障功能 ,肠源性内毒素移位及肠源性内毒血症的发生使病情进一步恶化
Objective: To investigate the dynamic changes of lipid peroxidation and nitric oxide (NO) in small intestine during secondary extra-pulmonary organ injury secondary to acute respiratory distress syndrome (ARDS). Methods: Rabbit model of ARDS was induced by oleic acid and divided into 30, 60, 90 and 120 m in4 groups. The levels of glutathione peroxidase (GPH-Px), malondialdehyde (MDA) ) And NO content. Results: (1) The contents of GPH-Px and MDA in small intestine of oleic acid group were significantly different from those in control group at each time point (P <0.05-0.01), and negative correlation was found between them = - 0.98, P <0 .01). (2) NO content in small intestine increased significantly in oleic acid 30 m in group than that in control group (P <0.01), but decreased in oleic acid 60 min group compared with oleic acid 30 min group (P <0.01). CONCLUSION: In the ARDS induced by oleic acid, the production of free radicals is increased, lipid peroxidation is induced, the production of NO is increased, and the function of various organs in the body is damaged. In particular, gastrointestinal barrier function, intestinal endotoxin translocation and intestinal The occurrence of sexual endotoxemia to further aggravate the condition