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在ＦｅＣｌ３损伤血管内皮导致的大鼠颈动脉血栓形成模型上发现血栓段血管组织环磷酸鸟苷（ｃＧＭＰ）含量减少，其内皮依赖性的乙酰胆碱（Ａｃｈ）扩血管作用减弱，而对非内皮依赖性的硝普钠扩血管反应无明显改变，病理形态观察可见动脉血栓形成和血管内皮严重损伤。用一氧化氮合成酶抑制剂ＬＮＮＡ处理后的动物明显地促进血栓形成，该作用可被一氧化氮前体Ｌ－精氦酸（Ｌ－Ａｒｇ）所拮抗，用Ｌ－Ａｒｇ处理后的动物显著减轻血栓形成，并部分恢复血管对Ａｃｈ的扩血管作用。提示，内皮舒张因子（Ｅｎｄｏｔｈｅｌｉｕｍ－ｄｅｒｉｖｅｄｒｅｌａｘｉｎｇｆａｃｔｏｒ，ＥＤＲＦ）可能是机体重要的内源性抗栓物质，在血栓性疾病的防治中具有重要意义。
In the rat model of carotid thrombosis induced by FeCl3-injured vascular endothelium, we found that the content of cyclic guanosine monophosphate (cGMP) decreased in the thrombus segment, and the endothelium-dependent acetylcholine (Ach) No significant changes were observed in the vasodilator response to sodium nitroprusside. Arterial thrombosis and severe vascular endothelial injury were observed in the pathological examination. Animals treated with LNNA, an inhibitor of nitric oxide synthase, significantly promoted thrombus formation, which was antagonized by L-Arg, a nitric oxide precursor, and animals treated with L-Arg were significantly Reduce thrombus formation, and partially restore the vascular vasodilator effect on Ach. It is suggested that endothelium-derived protective factor (EDRF) may be an important endogenous antithrombotic substance in the body, which is of great significance in the prevention and treatment of thrombotic diseases.