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目的：研究脂质过氧化损伤后内皮细胞产生环磷腺苷酸（ｃＡＭＰ）、一氧化氮（ＮＯ）的量的变化及ＮＯ形成过程中第二信使ｃＡＭＰ的作用。方法：用联胺、硒作为氧化剂及抗氧化剂，应用光镜、电镜、丙二醛测定方法观察内皮细胞脂质过氧化损伤程度；用放免方法测细胞内ｃＡＭＰ含量，Ｇｒｉｅｓｓ方法测培养液中ＮＯ代谢产物亚硝酸盐（ＮＯ－２）的含量。结果：联胺可以引起内皮细胞脂质过氧化损伤，低、中联胺浓度组ｃＡＭＰ含量明显升高，硒保护组比损伤组降低（Ｐ＜０．０１），高联胺浓度组ｃＡＭＰ降低，加硒组有所回升（Ｐ＜０．０５）。但ＮＯ含量随联胺浓度升高增多（Ｐ＜０．０１），硒可使ＮＯ升高程度减小（Ｐ＜０．０５）。ｃＡＭＰ升高因素可使内皮细胞（ＥＣ）产生ＮＯ增多。结论：轻中度或早期动脉硬化（ＡＳ）病变可能是通过ｃＡＭＰ介导的；ｃＡＭＰ可能在ＮＯ合成中起一定作用。以往ＮＯ“减少”的报道可能是由于产生的ＮＯ被自由基等灭活导致ＮＯ的活性降低
OBJECTIVE: To investigate the changes of cAMP and NO in endothelial cells after lipid peroxidation injury and the effect of cAMP, a second messenger in the process of NO formation. Methods: Using diamine and selenium as oxidants and antioxidants, the degree of lipid peroxidation in endothelial cells was observed by light microscopy, electron microscopy and malondialdehyde determination. The intracellular cAMP content was measured by radioimmunoassay and Grignard assay Metabolite nitrite (NO-2) content. Results: Hydrochloride induced lipid peroxidation injury in endothelial cells. The levels of cAMP in low and medium hydrazine groups were significantly higher than those in injured group (P <0.01) Selenium group has picked up (P <0.05). However, the content of NO increased with the increase of the concentration of diamine (P <0.01), and the level of NO increased with selenium (P <0.05). Elevated cAMP causes endothelial cells (EC) to produce increased NO. CONCLUSIONS: Lesions of mild to moderate or early atherosclerosis (AS) may be mediated by cAMP; cAMP may play a role in NO synthesis. Previous reports of “reduction” of NO may be due to a decrease in the NO activity resulting from the inactivation of NO by free radicals or the like