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Effects of l -Arginine on Fibroblast Growth Factor 2–Induced Angiogenesis in a Model of Endothelial Dysfunction
Author(s) -
Pierre Voisine,
Jian Li,
Cesario Bianchi,
Tanveer Ahmed Khan,
Marc Ruel,
Shuhua Xu,
Jun Feng,
Audrey Rosinberg,
Tamer Malik,
Yasunari Nakai,
Frank W. Sellke
Publication year - 2005
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.104.526350
Subject(s) - medicine , enos , fibroblast growth factor , endothelial dysfunction , angiogenesis , nitric oxide , endocrinology , endothelium , arginine , vascular endothelial growth factor , nitric oxide synthase , coronary artery disease , perfusion , endothelial stem cell , receptor , biochemistry , biology , in vitro , amino acid , vegf receptors
Nitric oxide availability, which is decreased in advanced coronary artery disease associated with endothelial dysfunction, is an important mediator of fibroblast growth factor-2 (FGF-2)-induced angiogenesis. This could explain the disappointing results of FGF-2 therapy in clinical trials despite promising preclinical studies. We examined the influence of L-arginine supplementation to FGF-2 therapy on myocardial microvascular reactivity and perfusion in a porcine model of endothelial dysfunction.

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