Kattlove H E, Gomez M H
Department of Medicine, Harbor General Hospital, Torrance, Calif. 90509.
Blood. 1975 Jan;45(1):91-6.
Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin-induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.
在瑞斯托霉素诱导的血小板聚集过程中，对腺嘌呤核苷酸代谢和释放反应进行了研究。通过与代谢毒物孵育降低血小板ATP水平，并未降低瑞斯托霉素诱导的聚集。在瑞斯托霉素诱导的聚集过程中，ADP和ATP从血小板中释放出来，且ATP转化为次黄嘌呤。然而，这些情况发生在聚集几乎完成之后。对氯汞苯甲酸可抑制聚集。通过研究血小板悬浮液，我们能够确定这种作用是针对血小板的，而非针对聚集所需的血浆辅因子。我们推测，瑞斯托霉素及其辅因子通过结合血小板膜使血小板聚集，并且血小板在该反应中起被动作用。
