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目的：观察肠缺血—再灌流过程中肠源性ＩＮＦα和ＩＬ－６ 表达的规律并探讨介导肠源性细胞因子表达的因素。方法：采用ＲＴ—ＰＣＲ和ＲＩＡ 的方法检测了肠缺血—再灌流过程中小肠组织ＴＮＦα和ＩＬ６ｍ ＲＮＡ表达及其蛋白含量的变化，并测定组织丙二醛（ＭＤＡ）含量及肠静脉血浆ＬＰＳ浓度。结果：正常情况下小肠ＴＮＦα和ＩＬ～６ｍ ＲＮＡ仅有少量表达，肠缺血１ｈ～１．５ｈ，表达已开始增加，再灌流０．５ｈ～１ｈ，表达至峰值，与肠静脉血浆内毒素（ＬＰＳ）浓度及组织丙二醛（ＭＤＡ）含量变化趋势基本一致，但表达增加的高峰略早于血浆ＬＰＳ峰值而晚于组织ＭＤＡ含量的增加。结论：肠缺血—再灌流时，肠道是早期产生炎性细胞因子的重要器官，在诱发ＳＩＲＳ中可能起重要作用；原发的缺氧、氧自由基生成及通过受损肠壁的ＬＰＳ可能均参与介导小肠炎性介质的表达。
OBJECTIVE: To observe the regularity of expression of INFa and IL-6 in intestinal ischemia-reperfusion and to explore the factors that may affect the expression of gut-derived cytokines. Methods: The expressions of TNFα and IL-6mRNA in small intestine during intestinal ischemia-reperfusion were detected by RT-PCR and RIA. The content of malondialdehyde (MDA) and the content of LPS in intestinal vein . Results: The expression of TNFα and IL-6mRNA in small intestine was only a small amount in normal condition. The intestinal ischemia increased from 1h to 1.5h and began to increase after 0.5h to 1h of reperfusion, LPS) and MDA content of the tissue were basically the same, but the peak of expression increased slightly earlier than the peak of plasma LPS and later than the increase of MDA content. CONCLUSIONS: During intestinal ischemia-reperfusion, the intestine is an important organ that produces inflammatory cytokines in the early stage and may play an important role in inducing SIRS. Primary hypoxia, generation of oxygen free radicals and passage of LPS May be involved in mediating the expression of inflammatory mediators in the small intestine.