高密度脂蛋白促进内皮衍生的一氧化氮抑制血小板聚集的作用

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

High density lipoproteins enhanced antiaggregating activity of nitric oxide derived from bovine aortal endothelial cells

In the present study, the effect of high density lipoproteins (HDLs) on the antiaggregating activity of nitric oxide (NO) derived from endothelial cells was investigated with the use of cultured bovine aortal endothelial cells (BAECs). The BAECs were placed in an aggregometer in contact with rabbit platelets after blocking cyclo-oxygenase with acetylsalicylic acid. Under this circumstance, the antiaggregating effect of endothelial cells was exclusively dependent on the release of NO, which was further confirmed by prevention of antiaggregating activity of BAECs with 1 mmol/L N(G)-Nitro-L-arginine. When this system was used, thrombin (0.1 U/ml) evoked 67.33+/-7.52% aggregation of rabbit platelets (2 10(8)/ml). This effect was inhibited by NO derived from endothelial cells (1 10(5) 1 10(6)/ml) in a cell number dependent manner. HDLs (1 mg/ml), added into the system immediately before BAECs, enhanced this antiaggregating effect of NO. However, incubating BAECs with HDLs for an hour and removing the HDLs by centrifugation did not have the same effect, unless HDLs were present during aggregation. No direct effect of HDLs on platelet aggregation was observed. The above findings suggest that HDLs can enhance the antiaggregating effects of BAECs mediated by direct interaction with NO.