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血小板聚集抑制剂作用的超微结构研究(作者译)

[Ultrastructural study on the effect of an inhibitor of platelet aggregation (author's transl)].

作者信息

Le Menn R, Migne J, Probst-Dvojakovic R J

出版信息

Arzneimittelforschung. 1979;29(8a):1278-82.

PMID:540072
Abstract

10-Methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) is introduced into human platelet-rich plasma at different stages of collagen-, ADP- or epinephrine-induced aggregation. Ultrastructural fixation is processed while aggregation on the same plasma sample is recorded. If introduced before the aggregating agent, nicergoline completely neutralises its action and the platelets become spherical. The microtubule marginal bundle is disorganized and both open and dense canalicular systems are modified. If intoduced after the aggregating agent, nicergoline immediately stops the aggregation and disaggregation follows, with complete separation of the platelets. Morphology of microtubules and canalicular systems depend on the time before application of nicergoline. Nicergoline stops the induction of aggregation as well as ADP release. Disaggregation is an active process involving the microtubules.

摘要

10-甲氧基-1,6-二甲基-麦角灵-8β-甲醇-(5-溴烟酸酯)(尼麦角林,喜得镇)在胶原、ADP或肾上腺素诱导的血小板聚集的不同阶段加入到富含血小板的人血浆中。在记录同一血浆样本聚集情况的同时进行超微结构固定。如果在聚集剂之前加入,尼麦角林可完全中和其作用,血小板变为球形。微管边缘束紊乱,开放和致密的小管系统均发生改变。如果在聚集剂之后加入,尼麦角林可立即停止聚集并随后发生解聚,血小板完全分离。微管和小管系统的形态取决于加入尼麦角林之前的时间。尼麦角林可阻止聚集诱导以及ADP释放。解聚是一个涉及微管的活跃过程。

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