Nunn B
Thromb Haemost. 1979 Dec 21;42(4):1193-206.
The hypothesis that platelet ADP is responsible for collagen-induced aggregation has been re-examined. It was found that the concentration of ADP obtaining in human PRP at the onset of aggregation was not sufficient to account for that aggregation. Furthermore, the time-course of collagen-induced release in human PRP was the same as that in sheep PRP where ADP does not cause release. These findings are not consistent with claims that ADP alone perpetuates a collagen-initiated release-aggregation-release sequence. The effects of high doses of collagen, which released 4-5 microM ADP, were not inhibited by 500 microM adenosine, a concentration that greatly reduced the effect of 300 microM ADP. Collagen caused aggregation in ADP-refractory PRP and in platelet suspensions unresponsive to 1 mM ADP. Thus human platelets can aggregate in response to collagen under circumstances in which they cannot respond to ADP. Apyrase inhibited aggregation and ATP release in platelet suspensions but not in human PRP. Evidence is presented that the means currently used to examine the role of ADP in aggregation require investigation.
血小板ADP导致胶原诱导聚集的假说已被重新审视。研究发现，在聚集开始时人富血小板血浆（PRP）中ADP的浓度不足以解释该聚集现象。此外，人PRP中胶原诱导释放的时间进程与绵羊PRP相同，而在绵羊PRP中ADP不会引起释放。这些发现与仅ADP能维持胶原引发的释放 - 聚集 - 释放序列的说法不一致。释放4 - 5微摩尔ADP的高剂量胶原的作用不受500微摩尔腺苷的抑制，该浓度能大大降低300微摩尔ADP的作用。胶原在对ADP不敏感的PRP和对1毫摩尔ADP无反应的血小板悬液中引起聚集。因此，人血小板在无法对ADP作出反应的情况下仍能对胶原作出聚集反应。腺苷三磷酸双磷酸酶抑制血小板悬液中的聚集和ATP释放，但不抑制人PRP中的聚集和ATP释放。有证据表明，目前用于研究ADP在聚集中作用的方法需要进行研究。
