胶原诱导的血小板聚集:腺嘌呤核苷酸的作用及其释放反应。

H Kattlove, M H Gomez
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引用次数: 0

摘要

胶原诱导的血小板聚集与ADP的释放和放射性ATP的分解代谢有关。这些研究表明,人血小板ADP的释放量和ATP的分解代谢量随着胶原-富血小板血浆(PRP)混合物的搅拌时间和胶原含量的增加而增加。腺嘌呤核苷酸的这些变化与聚集同时发生。未注意到聚合前的早期变化。搅拌胶原- prp混合物使ADP释放和ATP分解代谢最大化;一些ADP释放和ATP分解代谢发生在最小的躁动。PRP与代谢毒物(2-脱氧葡萄糖与KCN或寡霉素)孵育,可降低血小板ATP含量,也减少胶原诱导的ADP释放和聚集。然而,血小板粘附胶原蛋白不受代谢毒物的影响。这些数据表明胶原蛋白直接刺激ADP的释放。EDTA-PRP释放的证明进一步表明,胶原诱导的ADP释放不需要血小板聚集。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Collagen-induced platelet aggregation: the role of adenine nucleotides and the release reaction.

Collagen-induced platelet aggregation is associated with the release of ADP and the catabolism of radioactive ATP. These studies demonstrate that the amount of human platelet ADP released and ATP catabolized increase with time of stirring of the collagen-platelet rich plasma (PRP) mixture and with increasing amounts of collagen. These changes in adenine nucleotides occurred simultaneously with the aggregation. No early changes preceding aggregation were noted. Stirring the collagen-PRP mixture maximized ADP release and ATP catabolism; some ADP release and ATP catabolism occurred with minimal agitation. Incubation of PRP with metabolid poisons (2-deoxyglucose with either KCN or oligomycin), which lowered platelet ATP content, also reduced collagen-induced release of ADP and aggregation. However, platelet adhesion to collagen was unaffected by metabolic poisons. These data suggest that collagen directly stimulates ADP release. The demonstration of release in EDTA-PRP further suggest that platelet aggregation is not required for collagen-induced ADP release.

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