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阿司匹林对人血小板聚集的抑制作用及对一氧化氮合成的刺激作用。

Inhibition of human blood platelet aggregation and the stimulation of nitric oxide synthesis by aspirin.

作者信息

Chakraborty Kushal, Khan Gausal Azam, Banerjee Pratik, Ray Udayan, Sinha Asru K

机构信息

Sinha Institute of Medical Science and Technology, Calcutta, India.

出版信息

Platelets. 2003 Nov-Dec;14(7-8):421-7. doi: 10.1080/095371032000158763.

DOI:10.1080/095371032000158763
PMID:14713511
Abstract

Incubation of platelet-rich plasma with 80 microM aspirin that resulted in the inhibition of both the secondary phase of ADP induced platelet aggregation and prostaglandin synthesis simultaneously stimulated the production of NO in platelets. Furthermore it was found that the treatment of platelet-rich plasma either with 80 microM ibuprofen or salicylic acid, like aspirin, which inhibited the secondary phase of platelet aggregation by ADP and prostaglandin synthesis, also stimulated the production of NO in the absence of added ADP. However the inhibition of prostaglandin synthesis by ibuprofen or salicylic acid, unlike aspirin, was transient in nature. Incubation of washed platelets with any of these three compounds also stimulated NO synthesis indicating that the effect of these compounds was not mediated through plasma proteins. The in vitro effect of aspirin on the increase of NO in platelets could also be demonstrated by in vivo exposure of platelets to the compound. It was concluded that either a temporary or a lasting inhibition of prostaglandin synthesis by these inhibitors resulted in the synthesis of NO in resting platelets. Since NO is a potent inhibitor of platelet aggregation the inhibition of platelet aggregation, by these compounds may not be the consequence of the inhibition of prostaglandin synthesis alone, but could also be related, at least partly, to the stimulated synthesis of NO by these inhibitors.

摘要

富含血小板血浆与80微摩尔阿司匹林一起孵育,结果导致ADP诱导的血小板聚集的第二阶段和前列腺素合成同时受到抑制,同时刺激了血小板中一氧化氮(NO)的产生。此外,还发现用80微摩尔布洛芬或水杨酸处理富含血小板血浆,与阿司匹林一样,它们通过抑制ADP诱导的血小板聚集的第二阶段和前列腺素合成,在未添加ADP的情况下也刺激了NO的产生。然而,与阿司匹林不同,布洛芬或水杨酸对前列腺素合成的抑制本质上是短暂的。用这三种化合物中的任何一种孵育洗涤过的血小板也刺激了NO的合成,这表明这些化合物的作用不是通过血浆蛋白介导的。阿司匹林对血小板中NO增加的体外作用也可以通过血小板在体内接触该化合物来证明。得出的结论是,这些抑制剂对前列腺素合成的暂时或持久抑制导致了静息血小板中NO的合成。由于NO是血小板聚集的有效抑制剂,这些化合物对血小板聚集的抑制可能不仅仅是前列腺素合成抑制的结果,至少部分还可能与这些抑制剂刺激NO的合成有关。

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