Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins

F. Berti, G. Rossoni, G. Biasis, A. Buschi, V. Mandelli, C. Tondo

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Spirals of human saphenous veins (HSV), mounted in a 5 ml organ bath containing Krebs-Henseleit solution (37°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 (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. 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, 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 defibrptide, may have therapeutical value against immoderate changes of venous tone.

Original languageEnglish
Pages (from-to)337-350
Number of pages14
JournalProstaglandins
Volume40
Issue number4
DOIs
Publication statusPublished - 1990

Fingerprint

Saphenous Vein
Endothelin-1
Epoprostenol
Indomethacin
Tissue
Eicosanoids
Vasoconstrictor Agents
Prostaglandin-Endoperoxide Synthases
Dinoprostone
Metabolism
Washing
Prostaglandins
Modulation
Peptides
Baths
Enzymes
defibrotide
prostaglandin F1

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins. / Berti, F.; Rossoni, G.; Biasis, G.; Buschi, A.; Mandelli, V.; Tondo, C.

In: Prostaglandins, Vol. 40, No. 4, 1990, p. 337-350.

Research output: Contribution to journalArticle

Berti, F. ; Rossoni, G. ; Biasis, G. ; Buschi, A. ; Mandelli, V. ; Tondo, C. / Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins. In: Prostaglandins. 1990 ; Vol. 40, No. 4. pp. 337-350.
@article{d9c18606b80540da97804ec75e262818,
title = "Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins",
abstract = "Spirals of human saphenous veins (HSV), mounted in a 5 ml organ bath containing Krebs-Henseleit solution (37°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-PGF1α (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-PGF1α. 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-PGF1α, 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 defibrptide, may have therapeutical value against immoderate changes of venous tone.",
author = "F. Berti and G. Rossoni and G. Biasis and A. Buschi and V. Mandelli and C. Tondo",
year = "1990",
doi = "10.1016/0090-6980(90)90099-H",
language = "English",
volume = "40",
pages = "337--350",
journal = "Prostaglandins and Other Lipid Mediators",
issn = "1098-8823",
publisher = "Elsevier Inc.",
number = "4",

}

TY - JOUR

T1 - Defibrotide, by enhancing prostacyclin generation, prevents endothelin-1 induced contraction in human saphenous veins

AU - Berti, F.

AU - Rossoni, G.

AU - Biasis, G.

AU - Buschi, A.

AU - Mandelli, V.

AU - Tondo, C.

PY - 1990

Y1 - 1990

N2 - Spirals of human saphenous veins (HSV), mounted in a 5 ml organ bath containing Krebs-Henseleit solution (37°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-PGF1α (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-PGF1α. 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-PGF1α, 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 defibrptide, may have therapeutical value against immoderate changes of venous tone.

AB - Spirals of human saphenous veins (HSV), mounted in a 5 ml organ bath containing Krebs-Henseleit solution (37°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-PGF1α (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-PGF1α. 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-PGF1α, 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 defibrptide, may have therapeutical value against immoderate changes of venous tone.

UR - http://www.scopus.com/inward/record.url?scp=0025001566&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025001566&partnerID=8YFLogxK

U2 - 10.1016/0090-6980(90)90099-H

DO - 10.1016/0090-6980(90)90099-H

M3 - Article

VL - 40

SP - 337

EP - 350

JO - Prostaglandins and Other Lipid Mediators

JF - Prostaglandins and Other Lipid Mediators

SN - 1098-8823

IS - 4

ER -