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目的：观察肿瘤坏死因子（ＴＮＦ）、内源性一氧化氮（ＮＯ）和磷脂酶Ａ２（ＰＬＡ２）在大鼠小肠缺血再灌注（ＩＲ）所致肺损伤发病过程中的作用，及大黄对ＴＮＦ、ＮＯ和ＰＬＡ２的影响，探讨大黄防治肠源性肺损伤的机制。方法：ＳＤ大鼠随机分为肠缺血再灌注组、假手术组、大黄治疗组和安慰剂组。以１２５Ｉ标记小牛血清白蛋白（ＢＳＡ）肺摄取指数作为评价肺损伤的指标，以髓过氧化物酶（ＭＰＯ）作为评价多形核白细胞（ＰＭＮ）在组织中聚集的指标，分别测定各组动物不同时间血浆、肺组织ＴＮＦ含量，血浆（血清）、肺及小肠组织内源性ＮＯ含量及ＰＬＡ２活性。结果：大黄可显著改善ＩＲ导致的低血压状态并明显抑制再灌注导致的肺ＭＰＯ活性升高（Ｐ＜０．０１）；抑制肠缺血和再灌注早期出现的血浆及肺组织ＴＮＦ水平升高（Ｐ＜０．０１）；抑制肠缺血期和再灌注期血清、肺及小肠组织ＰＬＡ２活性升高（Ｐ＜０．０５或Ｐ＜０．０１）及再灌注期的内源性ＮＯ释放（Ｐ＜０．０５或Ｐ＜０．０１）；降低肺毛细血管通透性（Ｐ＜０．０１）。结论：缺血再灌注早期应用大黄能明显防治大鼠ＩＲ所致的肺损伤，这种作用可能是通过抑制ＴＮＦ、内源性ＮＯ及ＰＬＡ２等介质的释放实现的。
AIM: To observe the role of tumor necrosis factor (TNF), endogenous nitric oxide (NO) and phospholipase A2 (PLA2) in the pathogenesis of lung injury induced by intestinal ischemia-reperfusion (IR) TNF, NO and PLA2 to explore the mechanism of rhubarb prevention and treatment of gut-derived lung injury. Methods: SD rats were randomly divided into intestinal ischemia-reperfusion group, sham operation group, rhubarb treatment group and placebo group. 125I-labeled bovine serum albumin (BSA) pulmonary uptake index was used as an index to evaluate lung injury, and myeloperoxidase (MPO) was used as an index to evaluate the aggregation of polymorphonuclear leukocytes (PMN) in the tissues. Each group The content of TNF in plasma and lung tissue, plasma (serum), endogenous NO content in lung and small intestine and the activity of PLA2 in animal at different times. RESULTS: Rhubarb significantly improved the hypotensive state induced by IR and significantly inhibited the reperfusion-induced pulmonary MPO activity (P <0.01), and inhibited the increased levels of TNF in plasma and lung tissue during early stage of intestinal ischemia and reperfusion (P <0.01); inhibit the PLA2 activity (P <0.05 or P <0.01) and the release of endogenous NO in serum, lung and small intestine after intestinal ischemia and reperfusion (P <0.05 or P <0.01), decreased pulmonary capillary permeability (P <0.01). Conclusion: The application of rhubarb in the early stage of ischemia-reperfusion can prevent and cure lung injury induced by IR in rats. This effect may be achieved by inhibiting the release of TNF, endogenous NO and PLA2.