Biagi G, Legnani C, Rodorigo G, Coccheri S
Chair of Medical Pathophysiology, University Hospital S. Orsola, Bologna, Italy.
Arzneimittelforschung. 1991 May;41(5):511-4.
Acute intravenous administration in man of defibrotide (CAS 83712-60-1), a polynucleotide derivative, induces increase of 6-keto-PGF1 alpha and PGE2 production from appropriately stimulated whole blood. In the present study including acute and chronic experiments, defibrotide (Prociclide) orally administered during two weeks to healthy volunteers significantly increased the amounts of 6-keto-PGF1 alpha generated after appropriate stimulation in whole blood and in a neutrophilic leukocytes-platelet suspension. Similar effects were observed for PGE2, while TXB2 production was unchanged. Furthermore, platelet aggregation induced by calcium ionophore A23817 and production of leukotriene B4 from whole blood and isolated polymorphonuclear neutrophils were inhibited. The observed results suggest that defibrotide is biochemically active also by the oral route although the pharmacological and clinical value of the observed changes needs to be assessed.
多核苷酸衍生物去纤苷（CAS 83712 - 60 - 1）对人体进行急性静脉给药时，会使经适当刺激的全血中6 - 酮 - PGF1α和PGE2的生成量增加。在本项包括急性和慢性实验的研究中，健康志愿者连续两周口服去纤苷（普罗西克莱德）后，经适当刺激的全血以及嗜中性白细胞 - 血小板悬液中生成的6 - 酮 - PGF1α量显著增加。对PGE2也观察到类似效果，而TXB2的生成未发生变化。此外，钙离子载体A23817诱导的血小板聚集以及全血和分离出的多形核中性粒细胞中白三烯B4的生成受到抑制。观察结果表明，尽管所观察到的变化的药理学和临床价值有待评估，但去纤苷经口服途径也具有生化活性。
