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β受体阻滞剂在体外可抑制胎儿血栓素A2的生成。

Beta blockers inhibit fetal thromboxane A2 production in vitro.

作者信息

Viinikka L, Ylikorkala O

机构信息

Children's Hospital, University of Helsinki, Finland.

出版信息

Biol Neonate. 1988;54(3):169-72. doi: 10.1159/000242848.

Abstract

The effects of beta-blocking propranolol, metoprolol, atenolol and labetalol on the production of the proaggregatory and vasoconstrictive thromboxane A2 (TxA2) by fetal platelets were studied. To this end, umbilical blood samples were allowed to clot in the absence or presence of various concentrations of these agents, and the release of TxB2 (a metabolite of TxA2) was measured. Propranolol and labetalol inhibited TxA2 production in 0.1-mmol concentrations and metoprolol and atenolol in 1-mmol concentrations. The required concentration was always higher than could be achieved by peroral treatment. Beta blockers may have this effect through phospholipase A2 because the conversion of exogenous arachidonic acid to TxB2 was not affected except in the case of propranolol, which inhibited slightly TxB2 formation from exogenous arachidonic acid.

摘要

研究了β受体阻滞剂普萘洛尔、美托洛尔、阿替洛尔和拉贝洛尔对胎儿血小板产生促聚集和血管收缩性血栓素A2(TxA2)的影响。为此,让脐血样本在不存在或存在不同浓度这些药物的情况下凝固,并测量TxB2(TxA2的一种代谢产物)的释放量。普萘洛尔和拉贝洛尔在0.1毫摩尔浓度时抑制TxA2的产生,美托洛尔和阿替洛尔在1毫摩尔浓度时抑制TxA2的产生。所需浓度总是高于口服治疗所能达到的浓度。β受体阻滞剂可能通过磷脂酶A2产生这种作用,因为除了普萘洛尔略微抑制外源性花生四烯酸形成TxB2外,外源性花生四烯酸向TxB2的转化不受影响。

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