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Effects of L-arginine on fibroblast growth factor 2-induced angiogenesis in a model of endothelial dysfunction

Pierre Voisine1, Jian Li, Cesario Bianchi

  • 1Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. pierre.voisine@chg.ulaval.ca

Circulation
|September 15, 2005
PubMed
Abstract

Insights

L-arginine supplementation improved fibroblast growth factor-2 (FGF-2) therapy effectiveness in pigs with endothelial dysfunction. This combination therapy enhanced myocardial perfusion, suggesting a potential treatment for coronary artery disease.

Area of Science:

  • Cardiovascular Research
  • Vascular Biology
  • Regenerative Medicine

Background:

  • Endothelial dysfunction in coronary artery disease reduces nitric oxide availability, impairing fibroblast growth factor-2 (FGF-2)-induced angiogenesis.
  • Preclinical promise of FGF-2 therapy for angiogenesis has not translated to clinical success, possibly due to impaired nitric oxide pathways.

Purpose of the Study:

  • To investigate the impact of L-arginine supplementation on FGF-2 therapy in a porcine model of endothelial dysfunction.
  • To assess the effects on myocardial microvascular reactivity and perfusion.

Main Methods:

  • Pigs were fed high-cholesterol diets, with or without L-arginine, and underwent FGF-2 treatment after circumflex artery ameroid placement.
  • Coronary microvascular responses, myocardial perfusion, and protein levels (eNOS, iNOS) were assessed post-treatment.

Main Results:

  • High cholesterol induced endothelial dysfunction, which L-arginine normalized.
  • FGF-2 therapy alone was ineffective in improving myocardial perfusion in the high-cholesterol group.
  • L-arginine addition to FGF-2 therapy improved resting myocardial perfusion and increased eNOS and iNOS levels.

Conclusions:

  • L-arginine partially restored endothelial function and myocardial perfusion responses to FGF-2 in hypercholesterolemia-induced endothelial dysfunction.
  • Combination therapy with L-arginine and FGF-2 shows potential for treating end-stage coronary artery disease.

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