油酸致ARDS过程中小肠脂质过氧化和一氧化氮的动态变化

Dynamic changes of intestine lipid peroxidation and NO during oleic acid-induced ARDS

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 。

Objective: To study the dynamic changes and effect on the secondary organ injury of tissue lipid peroxidation and NO in ARDS. Methods: The ARDS model was made by oleic acid. Results: (1) The intestine GSH PX and MDA concentration showed marked discrepancy (P<0.05～0.01), and with positive correlation (r=-0.98, P<0.01) between oleic acid group and control. (2)Intestine NO concentration was markedly higher in 30 min than control (P<0.01), however, was lower in 90 min?120 min than in 30 min after CLP. Conclusion: In oleic acid induced ARDS, free radical induced more lipid peroxidation and NO, which resulted in organ injury. Especially, it decreased the gastroenteric function and increased the gastroenteric osmosis. The endotoxemia and infection originating from the gut deteriorated the disease.