Huang E M, Detwiler T C
J Lab Clin Med. 1980 Jan;95(1):59-68.
The observation that platelet secretion occurs in parallel with the second wave of platelet aggregation necessitates reassessment of the generally accepted concept that secreted ADP is the cause of second-wave aggregation. The major evidence for an involvement of secreted ADP is inhibition of second-wave aggregation by enzyme-catalyzed removal of ADP, interpreted as removal of secreted ADP. An alternative hypotheses, that the observed inhibition is due to a decrease in potentiation by extracellular ADP present prior to addition of stimulus, has been tested with the enzyme system CP plus CPK (CP/CPK). Low levels of CP/CPK inhibited gamma-thrombin-induced second-wave aggregation only after preincubation. When the second wave of gamma-thrombin- or epinephrine-induced aggregation was inhibited by very high levels of CP/CPK, the inhibition was overcome by an increase in the level of stimulus. These results are inconsistent with the idea that CP/CPK blocks second-wave aggregation by removing secreted ADP, but they are consistent with a decreased potentiation of the platelets due to a lower level of extracellular ADP prior to stimulation. Freshly prepared platelet-rich plasma contained a mean (n = 16) of 12 nM extracellular ADP. These data demonstrate that inhibition by CP/CPK cannot be taken as evidence for the involvement of secreted ADP.
血小板分泌与第二波血小板聚集同时发生这一观察结果，使得有必要重新评估普遍接受的观点，即分泌的ADP是第二波聚集的原因。支持分泌的ADP参与其中的主要证据是，通过酶催化去除ADP可抑制第二波聚集，这被解释为去除了分泌的ADP。另一种假说，即观察到的抑制是由于在添加刺激之前存在的细胞外ADP的增强作用降低，已通过酶系统CP加CPK（CP/CPK）进行了测试。低水平的CP/CPK仅在预孵育后才抑制γ-凝血酶诱导的第二波聚集。当γ-凝血酶或肾上腺素诱导的聚集的第二波被非常高水平的CP/CPK抑制时，通过增加刺激水平可克服这种抑制。这些结果与CP/CPK通过去除分泌的ADP来阻断第二波聚集的观点不一致，但与刺激前细胞外ADP水平较低导致血小板增强作用降低是一致的。新鲜制备的富含血小板血浆平均（n = 16）含有12 nM的细胞外ADP。这些数据表明，CP/CPK的抑制作用不能被视为分泌的ADP参与其中的证据。
