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目的：探讨肠系膜动脉闭塞性（ＳＭＡＯ）休克红细胞膜丙二醛（ＭＤＡ）水平及膜流动性变化，观察硫酸锌对其有无防治作用。方法：制备家兔肠系膜上动脉闭塞性休克模型，检测红细胞膜ＭＤＡ含量及膜流动性变化。实验分模型组、硫酸锌防治组和生理盐水（ＮＳ）对照组，并进行比较。结果：ＳＭＡＯ休克模型组红细胞膜ＭＤＡ水平明显高于防治组和ＮＳ对照组（Ｐ＜０．０１），红细胞膜流动性低于防治组和ＮＳ对照组；且模型组再灌注后ＭＤＡ含量与膜微粘度有直线正相关关系；防治组ＭＤＡ和膜流动性与对照组相比无显著性差异（Ｐ＞０．０５）。结论：红细胞膜ＭＤＡ水平是影响膜流动性重要原因，硫酸锌对肠系膜动脉闭塞休克有一定防治作用。红细胞膜脂质过氧化损伤是缺血／再灌注损伤的机制之一。
Objective: To investigate the level of malondialdehyde (MDA) and the membrane fluidity of erythrocyte membrane of SMAO rats and to observe the effect of zinc sulfate on them. Methods: The model of rabbit upper occlusive mesenteric artery occlusion was prepared and the content of MDA and membrane fluidity of erythrocyte membrane were measured. The experimental model group, zinc sulfate prevention group and normal saline (NS) control group, and compared. Results: The MDA level of erythrocyte membrane in SMAO shock model group was significantly higher than that in control group and NS control group (P <0.01), and the membrane fluidity of erythrocyte membrane was lower than that in control group and NS control group There was a linear positive correlation between microviscosity and control group. There was no significant difference in MDA and membrane fluidity between control group and control group (P> 0.05). Conclusion: The level of MDA in erythrocyte membrane is an important factor affecting membrane fluidity. Zinc sulfate has some preventive and therapeutic effects on mesenteric artery occlusion shock. Lipid peroxidation injury of erythrocyte membrane is one of the mechanisms of ischemia / reperfusion injury.