In vivo antithrombotic effect of triflavin, an Arg-Gly-Asp containing peptide on platelet plug formation in mesenteric microvessels of mice

J. R. Sheu, S. H. Chao, M. H. Yen, T. F. Huang

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. In this study, platelet thrombus formation was induced by irradiation of the mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Electron microscopy reveals moderately damaged endothelial cells, as well as aggregates consisting almost exclusively of platelets with pseudopod formation, and degranulated appearance. Triflavin (10-20 μg/g) significantly prolonged the lag period of inducing platelet plug formation in mesenteric venules when it was intravenously infused. Triflavin (20 μg/g) prolonged the occlusion time about 2-fold (from control 112 ± 23 to 240 ± 47 s). Furthermore, PGE1 briefly prolonged the occlusion time about 1.5-fold (from 105 ± 21 to 168 ± 20 s) when it was given by continuous infusion (40 μg/kg/min). On the other hand, triflavin was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at dose of 2-4 μg/g. Heparin (1.5 U/g) and indomethacin (200 μg/g) had no significant effect in prolonging the occlusion time or in reducing ADP-induced pulmonary embolism in mice. Therefore, triflavin is an effective antithrombotic agent in preventing the thromboembolism in these two in vivo models.

Original languageEnglish
Pages (from-to)617-621
Number of pages5
JournalThrombosis and Haemostasis
Volume72
Issue number4
Publication statusPublished - 1994
Externally publishedYes

Fingerprint

Microvessels
Blood Platelets
Peptides
Venules
Pulmonary Embolism
Adenosine Diphosphate
Snake Venoms
Pseudopodia
Fibrinolytic Agents
Alprostadil
Thromboembolism
Fluorescein
Platelet Aggregation
Indomethacin
Fibrinogen
Heparin
Electron Microscopy
Thrombosis
Endothelial Cells
triflavin

ASJC Scopus subject areas

  • Hematology

Cite this

In vivo antithrombotic effect of triflavin, an Arg-Gly-Asp containing peptide on platelet plug formation in mesenteric microvessels of mice. / Sheu, J. R.; Chao, S. H.; Yen, M. H.; Huang, T. F.

In: Thrombosis and Haemostasis, Vol. 72, No. 4, 1994, p. 617-621.

Research output: Contribution to journalArticle

@article{2ac29d3bd90040829c226c0a0b93f648,
title = "In vivo antithrombotic effect of triflavin, an Arg-Gly-Asp containing peptide on platelet plug formation in mesenteric microvessels of mice",
abstract = "Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. In this study, platelet thrombus formation was induced by irradiation of the mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Electron microscopy reveals moderately damaged endothelial cells, as well as aggregates consisting almost exclusively of platelets with pseudopod formation, and degranulated appearance. Triflavin (10-20 μg/g) significantly prolonged the lag period of inducing platelet plug formation in mesenteric venules when it was intravenously infused. Triflavin (20 μg/g) prolonged the occlusion time about 2-fold (from control 112 ± 23 to 240 ± 47 s). Furthermore, PGE1 briefly prolonged the occlusion time about 1.5-fold (from 105 ± 21 to 168 ± 20 s) when it was given by continuous infusion (40 μg/kg/min). On the other hand, triflavin was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at dose of 2-4 μg/g. Heparin (1.5 U/g) and indomethacin (200 μg/g) had no significant effect in prolonging the occlusion time or in reducing ADP-induced pulmonary embolism in mice. Therefore, triflavin is an effective antithrombotic agent in preventing the thromboembolism in these two in vivo models.",
author = "Sheu, {J. R.} and Chao, {S. H.} and Yen, {M. H.} and Huang, {T. F.}",
year = "1994",
language = "English",
volume = "72",
pages = "617--621",
journal = "Thrombosis and Haemostasis",
issn = "0340-6245",
publisher = "Schattauer GmbH",
number = "4",

}

TY - JOUR

T1 - In vivo antithrombotic effect of triflavin, an Arg-Gly-Asp containing peptide on platelet plug formation in mesenteric microvessels of mice

AU - Sheu, J. R.

AU - Chao, S. H.

AU - Yen, M. H.

AU - Huang, T. F.

PY - 1994

Y1 - 1994

N2 - Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. In this study, platelet thrombus formation was induced by irradiation of the mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Electron microscopy reveals moderately damaged endothelial cells, as well as aggregates consisting almost exclusively of platelets with pseudopod formation, and degranulated appearance. Triflavin (10-20 μg/g) significantly prolonged the lag period of inducing platelet plug formation in mesenteric venules when it was intravenously infused. Triflavin (20 μg/g) prolonged the occlusion time about 2-fold (from control 112 ± 23 to 240 ± 47 s). Furthermore, PGE1 briefly prolonged the occlusion time about 1.5-fold (from 105 ± 21 to 168 ± 20 s) when it was given by continuous infusion (40 μg/kg/min). On the other hand, triflavin was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at dose of 2-4 μg/g. Heparin (1.5 U/g) and indomethacin (200 μg/g) had no significant effect in prolonging the occlusion time or in reducing ADP-induced pulmonary embolism in mice. Therefore, triflavin is an effective antithrombotic agent in preventing the thromboembolism in these two in vivo models.

AB - Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. In this study, platelet thrombus formation was induced by irradiation of the mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Electron microscopy reveals moderately damaged endothelial cells, as well as aggregates consisting almost exclusively of platelets with pseudopod formation, and degranulated appearance. Triflavin (10-20 μg/g) significantly prolonged the lag period of inducing platelet plug formation in mesenteric venules when it was intravenously infused. Triflavin (20 μg/g) prolonged the occlusion time about 2-fold (from control 112 ± 23 to 240 ± 47 s). Furthermore, PGE1 briefly prolonged the occlusion time about 1.5-fold (from 105 ± 21 to 168 ± 20 s) when it was given by continuous infusion (40 μg/kg/min). On the other hand, triflavin was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at dose of 2-4 μg/g. Heparin (1.5 U/g) and indomethacin (200 μg/g) had no significant effect in prolonging the occlusion time or in reducing ADP-induced pulmonary embolism in mice. Therefore, triflavin is an effective antithrombotic agent in preventing the thromboembolism in these two in vivo models.

UR - http://www.scopus.com/inward/record.url?scp=0028040602&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028040602&partnerID=8YFLogxK

M3 - Article

C2 - 7878641

AN - SCOPUS:0028040602

VL - 72

SP - 617

EP - 621

JO - Thrombosis and Haemostasis

JF - Thrombosis and Haemostasis

SN - 0340-6245

IS - 4

ER -