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目的 :探讨 3 2 5℃～ 3 3℃低温对大鼠内毒素性急性肺损伤 (ALI)肺脂质过氧化的影响。方法 :采用大鼠腹腔注射内毒素 ,16h后再行气管内滴注内毒素的方法建立ALI模型。 2 4只雄性SD大鼠随机分为 3组 :正常对照组、内毒素组、低温组。ALI后 4h ,检测肺组织丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性。结果 :3组各时间点MAP、CVP相比无统计学意义 ( P>0 0 5)。内毒素组大鼠肺组织MDA含量显著高于正常对照组 ,SOD活性显著下降 ( P <0 0 5)。低温组SOD活性显著高于内毒素组 ,MDA含量也显著下降 (P <0 0 5) ,但与对照组相比无统计学意义 (P >0 0 5)。结论 :低温可减轻大鼠内毒素性急性肺损伤肺组织脂质过氧化。
Objective: To investigate the effect of low temperature (325 ℃ -333 ℃) on pulmonary lipid peroxidation in rats with acute lung injury induced by acute lung injury (ALI). Methods: The rat model of ALI was established by intraperitoneal injection of endotoxin and endotracheal intratracheal instillation after 16 hours. 24 male SD rats were randomly divided into 3 groups: normal control group, endotoxin group and hypothermia group. Four hours after ALI, the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in lung tissue were measured. Results: There were no significant differences in MAP and CVP between the three groups at all time points (P> 0.05). The content of MDA in lung tissue of endotoxin group was significantly higher than that of normal control group, and the activity of SOD was significantly decreased (P <0.05). The SOD activity in hypothermia group was significantly higher than that in endotoxin group, and the MDA content was also significantly decreased (P <0 05), but there was no significant difference compared with control group (P 0 05). Conclusion: Hypothermia can attenuate lipid peroxidation in lung tissue of rats with endotoxin-induced acute lung injury.