生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2000年
1期
81-84
,共4页
血小板聚集%高密度脂蛋白%内皮细胞%一氧化氮
血小闆聚集%高密度脂蛋白%內皮細胞%一氧化氮
혈소판취집%고밀도지단백%내피세포%일양화담
platelet aggregation%HDLs%nitric oxide%endothelial cells
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100μmol/L阿斯匹林处理,抑制细胞内的环氧化物酶活性.凝血酶(0.1 U/ml)可诱导兔血小板(2×108/ml) 67.33±7.52% 的聚集反应.内皮细胞(1×105～1×106/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1 mmol/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(1×105/ml)的这种作用.高密度脂蛋白(1mg/ml)与内皮细胞共同孵育1 h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.
用培養的小牛主動脈內皮細胞與兔水洗血小闆直接相互作用的模型,探討高密度脂蛋白對內皮衍生的一氧化氮抗血小闆聚集作用的影響.培養的小牛主動脈內皮細胞預先用100μmol/L阿斯匹林處理,抑製細胞內的環氧化物酶活性.凝血酶(0.1 U/ml)可誘導兔血小闆(2×108/ml) 67.33±7.52% 的聚集反應.內皮細胞(1×105～1×106/ml)能抑製凝血酶誘導的血小闆聚集,抑製彊度與內皮細胞的數目正相關.且此作用可被1 mmol/L硝基精氨痠完全取消.錶明內皮細胞對凝血酶誘導血小闆聚集的抑製作用都是由內皮衍生的一氧化氮所緻.在加凝血酶之前加入高密度脂蛋白(1mg/ml)可增彊內皮細胞(1×105/ml)的這種作用.高密度脂蛋白(1mg/ml)與內皮細胞共同孵育1 h後,將高密度脂蛋白離心棄去,內皮細胞對凝血酶誘導血小闆聚集的抑製作用不受影響.高密度脂蛋白及內皮細胞對靜息血小闆均無直接作用.結果錶明,高密度脂蛋白增彊內皮細胞抗凝血酶誘導的血小闆聚集反應的作用是通過直接作用于內皮衍生的一氧化氮而產生的.
용배양적소우주동맥내피세포여토수세혈소판직접상호작용적모형,탐토고밀도지단백대내피연생적일양화담항혈소판취집작용적영향.배양적소우주동맥내피세포예선용100μmol/L아사필림처리,억제세포내적배양화물매활성.응혈매(0.1 U/ml)가유도토혈소판(2×108/ml) 67.33±7.52% 적취집반응.내피세포(1×105～1×106/ml)능억제응혈매유도적혈소판취집,억제강도여내피세포적수목정상관.차차작용가피1 mmol/L초기정안산완전취소.표명내피세포대응혈매유도혈소판취집적억제작용도시유내피연생적일양화담소치.재가응혈매지전가입고밀도지단백(1mg/ml)가증강내피세포(1×105/ml)적저충작용.고밀도지단백(1mg/ml)여내피세포공동부육1 h후,장고밀도지단백리심기거,내피세포대응혈매유도혈소판취집적억제작용불수영향.고밀도지단백급내피세포대정식혈소판균무직접작용.결과표명,고밀도지단백증강내피세포항응혈매유도적혈소판취집반응적작용시통과직접작용우내피연생적일양화담이산생적.
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 NG-Nitro-L-arginine. When this system was used, thrombin (0.1 U/ml) evoked 67.33±7.52% aggregation of rabbit platelets (2×108/ml). This effect was inhibited by NO derived from endothelial cells (1×105～1×106/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.
