Terres W, Becker B F, Kratzer M A, Gerlach E
Thromb Res. 1986 May 15;42(4):539-48. doi: 10.1016/0049-3848(86)90217-3.
The time course of ADP induced aggregation of human platelets was determined in aliquots of stored platelet rich plasma 3.5, 10, 30 and 100 minutes after venepuncture. The maximal rate of aggregation was found to increase throughout this entire period, even though pH (7.4), CO2 (7 volume per cent) and temperature (35 degrees C) of the samples were kept constant. The mean acceleration (+/- SEM) between 3.5 and 100 minutes was 41.7 +/- 6.9 per cent (n = 67) at an ADP-concentration of 1 mumol/l and 18.3 +/- 6.2 per cent (n = 23) at 2 mumol/l ADP. The effect did not result from changes of any platelet regulatory factors putatively present alone in the plasma. Acceleration of aggregability was only found when the platelets themselves underwent storage, but not when freshly prepared plasma was given to prestored platelets. The change in aggregability was not diminished after inhibition of platelet cyclooxygenase by oral administration of acetylsalicylic acid.
在静脉穿刺后3.5、10、30和100分钟时，测定富血小板血浆样本中ADP诱导的人血小板聚集的时间进程。尽管样本的pH值（7.4）、二氧化碳含量（7%体积）和温度（35摄氏度）保持恒定，但在整个时间段内，最大聚集率均呈上升趋势。在1μmol/l ADP浓度下，3.5至100分钟之间的平均加速率（±SEM）为41.7±6.9%（n = 67），在2μmol/l ADP浓度下为18.3±6.2%（n = 23）。该效应并非由血浆中单独存在的任何血小板调节因子的变化引起。仅当血小板自身储存时，才发现聚集能力加速，而将新鲜制备的血浆给予预先储存的血小板时则未发现此现象。口服乙酰水杨酸抑制血小板环氧化酶后，聚集能力的变化并未减弱。
