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目的观察维生素E（VE）对急性胰腺炎（AP）时肺组织脂质过氧化的保护作用。方法采用3％牛磺胆酸钠按O1mg／kg体重注入胰管内制成AP动物模型后，经肠系膜静脉按100mg／kg体重注入VE乳剂或相同体积的生理盐水，术后6小时和24小时活杀动物检测血清淀粉酶、脂肪酸及磷脂酶A_2（PLA_2）活性；肺脏组织丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性及三磷酸腺着（ATP）含量。结果VE组动物肺脏组织炎性病理改变较AP组明显减轻；血清淀粉酶、脂肪酶及PLA_2活性均较AP组显著降低（P＜0．05）。肺脏组织MDA含量较AP组巳著降低（P＜0．05），SOD活性及ATP含量较AP组显著升高（P＜0.05）。结论氧自由基所引发的脂质过氧化作用是急性胰腺炎时肺脏损害发病过程中的重要因素之一，应用较大剂量VE可减轻肺脏组织损害。
Objective To observe the protective effect of vitamin E (VE) on lipid peroxidation of lung tissue in acute pancreatitis (AP). Methods 3% sodium taurocholate was injected into the pancreatic duct at O1mg / kg body weight to establish an animal model of AP. The rats were injected with VE emulsion or the same volume of normal saline via the mesenteric vein at a dose of 100mg / kg body weight. Six hours and 24 hours after the operation Animals were killed to test the activity of serum amylase, fatty acid and phospholipase A 2 (PLA 2), the content of malondialdehyde (MDA), the activity of superoxide dismutase (SOD) and the contents of triphosphate (ATP) in the lung tissue. Results The pathological changes of lung tissue in VE group were significantly reduced compared with those in AP group. The activities of serum amylase, lipase and PLA 2 were significantly lower than those in AP group (P <0.05). The content of MDA in lung tissue was lower than that in AP group (P <0.05), while the activity of SOD and the content of ATP in lung tissue were significantly higher than those in AP group (P <0.05). Conclusion Lipid peroxidation induced by oxygen free radicals is one of the important factors in the pathogenesis of lung injury in acute pancreatitis. Applying larger doses of VE can reduce lung tissue damage.