Institute of Anatomy, University of Münster, Vesaliusweg 2-4, W-4400, Münster, FR, Germany.
Platelets. 1993;4(1):41-4. doi: 10.3109/09537109309013194.
The isolated low density lipoprotein (LDL) has been shown to cause shape change, granule centralization and incomplete degranulation of human blood platelets at concentrations of 50 to 300 μg protein/ml in vitro. About half the number of platelets were discoid at the LDL concentration of 50 μg/ml. If the platelets were pretreated with LDL at a concentration of 100 μg/ml, aggregation could be induced by thrombin (0.015 U/ml) lightly. These results suggested that the LDL-incubated platelets showed a primary activation. These LDL-pretreated platelets showed enhanced sensitivity to thrombin by aggregating at a very low dosage (0.015 U/ml). The primary activation of platelets induced by LDL seemed independent of extracellular calcium when LDL concentrations were higher than 200 μg/ml.
体外实验表明，分离的低密度脂蛋白（LDL）在浓度为 50 至 300μg 蛋白/ml 时，可引起人血血小板形态改变、颗粒中心化和不完全脱颗粒。在 LDL 浓度为 50μg/ml 时，大约有一半的血小板呈盘状。如果血小板先用浓度为 100μg/ml 的 LDL 预处理，则可轻度诱导由凝血酶（0.015U/ml）引起的聚集。这些结果表明，LDL 孵育的血小板表现出初级激活。这些经 LDL 预处理的血小板在非常低的剂量（0.015U/ml）下聚集，显示出对凝血酶的敏感性增强。当 LDL 浓度高于 200μg/ml 时，LDL 诱导的血小板初级激活似乎与细胞外钙无关。
