双嘧达莫抑制氧衍生自由基诱导的血小板聚集。

Dipyridamole inhibits platelet aggregation induced by oxygen-derived free radicals.

作者信息

De la Cruz J P, García P J, Sánchez de la Cuesta F

机构信息

Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.

出版信息

Thromb Res. 1992 May 15;66(4):277-85. doi: 10.1016/0049-3848(92)90278-i.

DOI:10.1016/0049-3848(92)90278-i

PMID:1329255

Abstract

Pyrogallol (a generator of superoxide anions) caused 50% increase in platelet aggregation induced by 400 microM of arachidonic acid. Dipyridamole did not produce a statistically significant inhibition of arachidonic-acid induced platelet aggregation, but it caused 100% inhibition of pyrogallol-stimulated platelet aggregation. Ferrous salts (Fe2+) induced 34% platelet aggregation which was inhibited (79.6%) by a concentration of dipyridamole of 10 microM. Dipyridamole inhibited ferrous-induced lipid peroxidation with IC-50 values of 17.5 microM. When arachidonic acid was used as aggregating agent, the corresponding IC-50 value was 140.5 microM. These results indicate that dipyridamole prevented platelet activation induced by oxygen-derived free radicals.

摘要

连苯三酚（超氧阴离子生成剂）使由400微摩尔花生四烯酸诱导的血小板聚集增加50%。双嘧达莫对花生四烯酸诱导的血小板聚集未产生统计学上显著的抑制作用，但它对连苯三酚刺激的血小板聚集产生100%的抑制作用。亚铁盐（Fe2+）诱导34%的血小板聚集，10微摩尔浓度的双嘧达莫可抑制该聚集（79.6%）。双嘧达莫抑制亚铁诱导的脂质过氧化，IC-50值为17.5微摩尔。当使用花生四烯酸作为聚集剂时，相应的IC-50值为140.5微摩尔。这些结果表明双嘧达莫可防止由氧衍生的自由基诱导的血小板活化。