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Related Experiment Videos

Nicotine promotes arteriogenesis.

Christopher Heeschen1, Michael Weis, John P Cooke

  • 1Division of Cardiovascular Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305-5406, USA.

Journal of the American College of Cardiology
|February 11, 2003
PubMed
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Nicotine promotes blood vessel growth (angiogenesis and arteriogenesis) in ischemic limbs, comparable to basic fibroblast growth factor (bFGF). This effect may involve enhanced endothelial-monocyte interactions.

Area of Science:

  • Vascular biology and regenerative medicine
  • Pharmacology of angiogenesis and arteriogenesis

Background:

  • Nicotine has previously been shown to stimulate angiogenesis through endothelial nicotinic cholinergic receptors.
  • This stimulation leads to endothelial cell proliferation, migration, and capillary network formation in vitro and in vivo.

Purpose of the Study:

  • To evaluate nicotine's potential to enhance arteriogenesis in a limb ischemia model.
  • To compare nicotine's effect to basic fibroblast growth factor (bFGF).
  • To investigate the underlying mechanisms of nicotine's effect on arteriogenesis.

Main Methods:

  • Rabbits with unilateral femoral artery occlusion were treated with intra-arterial nicotine, bFGF, or vehicle.
  • Morphological changes were assessed using immunohistochemistry and angiography at day 21.

Related Experiment Videos

  • Blood flow was measured via Doppler and microsphere distribution.

    • Main Results:

    • Nicotine significantly increased capillary density in ischemic limbs, similar to bFGF.
    • Nicotine improved angiographic scores, calf blood pressure ratio, Doppler flow, and microsphere distribution.
    • In vitro studies showed nicotine enhanced monocyte adhesion and transmigration, upregulating key adhesion molecules and chemoattractant release.

    Conclusions:

    • Nicotine demonstrates short-term efficacy in promoting angiogenesis and arteriogenesis in ischemic conditions.
    • The pro-angiogenic and pro-arteriogenic effects of nicotine appear to be partly mediated by the activation of endothelial-monocyte interactions.