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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
08:42

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Published on: October 22, 2014

Basal and flow-mediated nitric oxide production by atheromatous coronary arteries

D Tousoulis1, C Tentolouris, T Crake

  • 1Cardiology Unit, Hippokration Hospital, Athens University Medical School, Greece.

Journal of the American College of Cardiology
|May 1, 1997
PubMed

Insights

Coronary artery dilation during increased heart rate relies on nitric oxide (NO). Inhibiting NO synthesis blocks this dilation in both normal and diseased human coronary arteries, confirming NO

Area of Science:

  • Cardiovascular physiology
  • Vascular biology
  • Nitric oxide research

Background:

  • Epicardial coronary arteries dilate with increased heart rate.
  • The role of nitric oxide in this dilation for human coronary arteries (normal and diseased) is unclear.

Purpose of the Study:

  • To investigate the effect of inhibiting nitric oxide synthesis on human epicardial coronary arteries.
  • To assess the impact on coronary flow velocity during baseline and atrial pacing.

Main Methods:

  • Intracoronary infusion of NG-monomethyl-L-arginine (LNMMA), a nitric oxide synthesis inhibitor.
  • Quantitative angiography to measure epicardial coronary artery lumen diameter.
  • Doppler catheter to measure coronary blood flow velocity during atrial pacing.

Main Results:

  • Atrial pacing increased lumen diameter during saline infusion but not during LNMMA infusion.
  • Coronary blood flow velocity changes with pacing were reduced when nitric oxide synthesis was inhibited.
  • Nitric oxide production was present at stenosis sites but unaffected by pacing.

Conclusions:

  • Epicardial coronary artery dilation due to pacing is dependent on nitric oxide.
  • Nitric oxide contributes significantly to the vasomotor tone of coronary resistance vessels.
  • Nitric oxide is produced in stenotic lesions, independent of pacing stimuli.
Abstract

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