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  • Title: Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins.
    Author: Berti F, Rossoni G, Biasi G, Buschi A, Mandelli V, Tondo C.
    Journal: Prostaglandins; 1990 Oct; 40(4):337-50. PubMed ID: 2126384.
    Abstract:
    Spirals of human saphenous veins (HSV), mounted in a 5 ml organ bath containing Krebs-Henseleit solution (37 degrees C), when kept in contact with defibrotide (100-200 ug/ml) for 15 min, enhance (2 and 3 fold) their own basal release of 6-keto-PGF 1 alpha (61 +/- 1.3 pg/mg w.t. n = 12). The phenomenon was long lasting upon repeated washing and sensitive to indomethacin (1 ug/ml). Endothelin-1 (ET-1, 20-40 ng) induced a sustained contraction of HSV and concomitantly released from the venous tissue a proportional amount of 6-keto-PGF 1 alpha. Indomethacin (1 ug/ml), by inhibiting cyclo-oxygenase enzyme, potentiated the contractile activity of ET-1 in HSV whereas exogenous PGE2 (20 ng/ml) considerably reduced the tension developed by the peptide on this venous tissue. Defibrotide (200 ug/ml), by releasing 6-keto-PGF 1 alpha, and other vasoactive prostaglandins, antagonized the contractile effect ET-1 (20 ng) in HSV. This data indicates that the eicosanoid metabolism is involved in the modulation of the potent vasoconstrictor effect of ET-1 in HSV and that PGI2-releaser, such as defibrotide, may have therapeutical value against immoderate changes of venous tone.
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