用培养的小牛主动脉内皮细胞与兔水洗血小板直接相互作用的模型 ,探讨高密度脂蛋白对内皮衍生的一氧化氮抗血小板聚集作用的影响。培养的小牛主动脉内皮细胞预先用 10 0 μmol/L阿斯匹林处理 ,抑制细胞内的环氧化物酶活性。凝血酶 ( 0 1U/ml)可诱导兔血小板 ( 2× 10 8/ml) 67 3 3± 7 5 2 %的聚集反应。内皮细胞 ( 1× 10 5～ 1× 10 6 /ml)能抑制凝血酶诱导的血小板聚集 ,抑制强度与内皮细胞的数目正相关。且此作用可被 1mmol/L硝基精氨酸完全取消。表明内皮细胞对凝血酶诱导血小板聚集的抑制作用都是由内皮衍生的一氧化氮所致。在加凝血酶之前加入高密度脂蛋白 ( 1mg/ml)可增强内皮细胞 ( 1× 10 5/ml)的这种作用。高密度脂蛋白 ( 1mg/ml)与内皮细胞共同孵育 1h后 ,将高密度脂蛋白离心弃去 ,内皮细胞对凝血酶诱导血小板聚集的抑制作用不受影响。高密度脂蛋白及内皮细胞对静息血小板均无直接作用。结果表明 ,高密度脂蛋白增强内皮细胞抗凝血酶诱导的血小板聚集反应的作用是通过直接作用于内皮衍生的一氧化氮而产生的 To investigate the effect of high density lipoprotein on endothelial derived anti-platelet aggregation of nitric oxide by using a model of direct interaction between cultured aorta endothelial cells and washed rabbit platelets. Cultured aortic endothelial cells were previously treated with aspirin at 10 μmol / L to inhibit intracellular epoxidase activity. Thrombin (0 1 U / ml) induces a 67 3 3 ± 75 2% aggregation of rabbit platelets (2 × 10 8 / ml). Endothelial cells (1 × 10 5 ~ 1 × 10 6 / ml) can inhibit thrombin-induced platelet aggregation, the intensity of inhibition is positively correlated with the number of endothelial cells. This effect can be completely abolished by 1 mmol / L nitro arginine. This indicates that the inhibitory effect of endothelial cells on thrombin-induced platelet aggregation is caused by endothelium-derived nitric oxide. Addition of high-density lipoprotein (1 mg / ml) before thrombin increases this effect of endothelial cells (1 x 10 5 / ml). After high-density lipoprotein (1 mg / ml) was incubated with endothelial cells for 1 h, high-density lipoprotein was centrifuged and discarded. The inhibitory effect of endothelial cells on thrombin-induced platelet aggregation was not affected. High density lipoprotein and endothelial cells have no direct effect on resting platelets. The results show that high-density lipoprotein enhances endothelial cell antithrombin-induced platelet aggregation by acting directly on endothelial-derived nitric oxide