Ts'ao C H
Scand J Haematol. 1975 Oct;15(3):171-7. doi: 10.1111/j.1600-0609.1975.tb01071.x.
Biphasic collagen-induced platelet aggregation, resembling that induced by epinephrine, was noted in platelet-rich plasma (PRP) of 11 stroke and 1 coronary disease patients. Similar pattern of aggregation was not observed in normal PRP. The occurrence of the biphasic collagen aggregation does not appear to relate to platelet count, smoking habit, medication, or other abnormalities such as hypertension, diabetes, and elevated serum lipid levels. However, platelets of these patients were very sensitive to aggregating agents including epinephrine and adenosine diphosphate. The concentration of collagen that elicited biphasic aggregation in these platelets was too weak to aggregate platelets of normal subjects. We believe that the release threshold of these platelets is reduced to such an extent that minute amounts of collagen, which would be insufficient to induce release from normal platelets, are capable of inducing release from these platelets. Both phases of collagen induced aggregation are probably resulted from the activation of the release mechanism.
在11名中风患者和1名冠心病患者的富血小板血浆（PRP）中，观察到双相胶原诱导的血小板聚集，类似于肾上腺素诱导的血小板聚集。在正常PRP中未观察到类似的聚集模式。双相胶原聚集的发生似乎与血小板计数、吸烟习惯、药物治疗或其他异常情况（如高血压、糖尿病和血脂升高）无关。然而，这些患者的血小板对包括肾上腺素和二磷酸腺苷在内的聚集剂非常敏感。在这些血小板中引发双相聚集的胶原浓度太弱，不足以使正常受试者的血小板聚集。我们认为，这些血小板的释放阈值降低到了这样的程度，即微量的胶原（不足以诱导正常血小板释放）能够诱导这些血小板释放。胶原诱导聚集的两个阶段可能都是由释放机制的激活导致的。
