Poller L, Thomson J M, Priest C M
Br Med J. 1969 Feb 22;1(5642):474-6. doi: 10.1136/bmj.1.5642.474.
Platelet aggregation has been related to blood coagulation studies in patients on nicoumalone, a coumarin anticoagulant. Aggregation studies were performed by means of Chandler's tube and the adenosine diphosphate (A.D.P.)-induced optical density method. Platelet aggregation in Chandler's tube has been shown to be quite different from A.D.P. aggregation and to be dependent on the "intrinsic" (blood) clotting system. When the intrinsic system was depressed by coumarin anticoagulant, aggregation was delayed in Chandler's tube, but patients with a predominantly "extrinsic" (tissue) system defect gave normal results even when their prothrombin time was excessively prolonged. In contrast there was an increased response to A.D.P. in the anticoagulated patients.The study emphasizes the different mechanisms of platelet aggregation, which we have referred to as coagulation-induced and A.D.P.-induced aggregation. It also shows the limitations of routine control of oral anticoagulants by prothrombin time alone, as the coagulation-induced platelet aggregation appears to be quantitatively related to the overall level of clotting factors in the intrinsic system and independent of the extrinsic system.
血小板聚集与服用香豆素类抗凝剂尼可香豆素患者的凝血研究有关。采用钱德勒管和二磷酸腺苷(ADP)诱导的光密度法进行聚集研究。钱德勒管中的血小板聚集已被证明与ADP聚集有很大不同,并且依赖于“内源性”(血液)凝血系统。当内源性系统被香豆素类抗凝剂抑制时,钱德勒管中的聚集会延迟,但主要存在“外源性”(组织)系统缺陷的患者即使其凝血酶原时间过度延长,结果仍正常。相比之下,抗凝患者对ADP的反应增强。该研究强调了血小板聚集的不同机制,我们将其称为凝血诱导聚集和ADP诱导聚集。它还表明仅通过凝血酶原时间对口服抗凝剂进行常规控制存在局限性,因为凝血诱导的血小板聚集似乎在数量上与内源性系统中凝血因子的总体水平相关,且与外源性系统无关。