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目的和方法：应用肝脏原位灌注模型，观察内皮素－１（ｅｎｄｏｔｈｅｌｉｎ－１，ＥＴ－１）对肝脏的损伤作用，以及一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）和前列环素（ｐｒｏｓｔａｃｙｃｌｉｎ，ＰＧＩ２）对ＥＴ－１生物学效应的调节作用。结果：ＥＴ－１能使肝细胞浊肿变性，增加脂质过氧化物生成和酶的漏出。ＮＯ合成抑制剂能使ＥＴ－１的肝损伤作用加重，ＰＧＩ２和消炎痛能部分减轻ＥＴ－１的肝损伤作用。结论：ＮＯ、ＰＧＩ２对ＥＴ－１的生物学效应并有一定的调节作用
PURPOSE AND METHODS: The hepatic injury was induced by endothelin-1 (ET-1) and the effects of nitric oxide (NO) and prostacyclin (PGI2) ET-1 biological effects of the regulatory role. Results: ET-1 could degenerate hepatocellular carcinoma and increase lipid peroxidation and enzyme leakage. NO synthesis inhibitors can aggravate the liver injury of ET-1, and PGI2 and indomethacin can partially reduce the liver injury of ET-1. CONCLUSION: The biological effects of NO and PGI2 on ET-1 have some regulatory effects