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目的探讨淋巴因子激活的杀伤细胞（ＬＡＫ细胞）与一氧化氮样内皮依赖性舒血管因子（ＥＤＲＦ）作用的相关性。方法动态观察自发性高血压大鼠（ＳＨＲ，ｎ＝５）ＬＡＫ细胞的增殖、活性及其所表达的ＳＯＤ样物质活性当量、自由基清除效应。同时观察胸主动脉环对乙酰胆碱（Ａｃｈ）的舒张反应，以及上述ＬＡＫ细胞与ＳＯＤ标准品对主动脉环（ｎ＝３０）的Ａｃｈ舒张反应的影响，与等量ＷＫＹ大鼠比较。结果与ＷＫＹ比，ＳＨＲ的ＬＡＫ细胞增殖、活性及其所表达的ＳＯＤ样物质和其自由基清除效应均明显降低（Ｐ＜０．０５），经ＬＡＫ细胞（无论来自ＷＫＹ还是ＳＨＲ）孵育后的主动脉环对Ａｃｈ的舒张反应均有不同程度增加。标准ＳＯＤ与ＬＡＫ细胞有相同效应。结论ＬＡＫ细胞可能通过表达ＳＯＤ样物质来减少ＮＯ氧化分解从而增强主动脉环的ＮＯ样舒血管作用。
Objective To investigate the relationship between lymphokine-activated killer (LAK) cells and nitric oxide-like endothelium-dependent vasodilator (EDRF). Methods The proliferation and activity of LAK cells in spontaneously hypertensive rats (SHR, n = 5) were dynamically observed, and the activity equivalent of SOD and the scavenging effect of free radicals on them were observed. At the same time, the effects of thoracic aortic rings on the relaxation of acetylcholine (Ach) and the Ach relaxation of aortic rings (n = 30) were compared between LAK cells and SOD standards, compared with WKY rats. Results Compared with WKY, the proliferation and activity of LAK cells in SHR and the activities of SOD-like substances and free radical scavengers in SHR were significantly decreased (P <0.05). After LAK cells (either from WKY or SHR) Aortic ring Ach relaxation response was increased to varying degrees. Standard SOD has the same effect as LAK cells. Conclusions LAK cells may reduce NO oxidation and decomposition and enhance the NO-like vasodilatation of the aortic rings by expressing SOD-like substances.