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[前列腺素和环核苷酸在药物性血小板减少症发病机制中的作用]

[Role of prostaglandins and cyclic nucleotides in the mechanism of development of drug-induced thrombocytopenia].

作者信息

Abesadze A I, Atanelishvili L I, Akhmeteli L I, Kvernadze M G, Mdivnishvili M G

出版信息

Biull Eksp Biol Med. 1993 Apr;115(4):354-6.

PMID:8049388
Abstract

The experiments on dogs have shown that at the moment of maximal thrombocytopenia, induced by using of 0.7 mg/kg rubomycin intravenous daily during 5 days, there was a sharp increase in cAMP concentration, while the content of prostaglandin E group and F2 alpha in blood decreased. Concentration of cGMP began to increase by the 10th day. We can arrive at the opinion that the rubomycin acts on the receptors of hemopoietic precursor cells' membrane. This causes the activation of adenylate-cyclase, which stimulates the formation of cAMP, causing cells' proliferation depression. This mechanism may be regarded as the restoration reaction of megakaryocyte-thrombocyte system.

摘要

对狗的实验表明,在连续5天每天静脉注射0.7mg/kg柔红霉素诱导产生最大血小板减少症时,环磷酸腺苷(cAMP)浓度急剧上升,而血液中前列腺素E组和F2α的含量下降。到第10天时,环磷酸鸟苷(cGMP)浓度开始上升。我们可以得出这样的观点,即柔红霉素作用于造血前体细胞的细胞膜受体。这会导致腺苷酸环化酶的激活,从而刺激cAMP的形成,导致细胞增殖受到抑制。这种机制可被视为巨核细胞-血小板系统的恢复反应。

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