title: Basal and flow-mediated nitric oxide production by atheromatous coronary arteries.
abstract: OBJECTIVE
  This study assessed the effects of inhibition of nitric oxide synthesis on epicardial human coronary arteries and on coronary flow velocity during baseline conditions and during atrial pacing.
  
  
  BACKGROUND
  Epicardial coronary artery dilation occurs in response to an increase in heart rate. It is not known whether the dilation of both angiographically normal and diseased epicardial coronary arteries during atrial pacing is nitric oxide dependent in humans.
  
  
  METHODS
  The effects of an intracoronary infusion (4 mumol/min for 8 min) of NG-monomethyl-L-arginine (LNMMA), an inhibitor of nitric oxide synthesis, was studied in 16 patients with coronary artery disease and in 6 patients with normal coronary arteriograms. In all patients atrial pacing was performed during normal saline and during LNMMA infusion. the lumen diameter of epicardial coronary arteries was assessed by quantitative angiography, and changes in blood flow velocity were measured with a Doppler catheter.
  
  
  RESULTS
  During saline infusion a significant increase in the lumen diameter of the proximal (p < 0.05) and distal (p < 0.01) segments of both normal and diseased arteries occurred during atrial pacing. No significant lumen diameter changes occurred in either group when atrial pacing was performed during LNMMA infusion. Stenosis diameter decreased during LNMMA infusion but did not change with atrial pacing either during saline infusion or during LNMMA infusion. The mean percent change in coronary blood flow with atrial pacing was less (p < 0.05) during LNMMA infusion than during saline infusion in both groups.
  
  
  CONCLUSIONS
  These findings confirm that epicardial coronary artery dilation induced by pacing is nitric oxide dependent. Nitric oxide production contributes to the vasomotor tone of coronary resistance vessels. Nitric oxide is produced at the site of atheromatous stenosis but is unaffected by pacing.
authors.affiliation: Cardiology Unit, Hippokration Hospital, Athens University Medical School, Greece.
authors.forename: D
authors.initials: D
authors.lastname: Tousoulis
authors.forename: C
authors.initials: C
authors.lastname: Tentolouris
authors.forename: T
authors.initials: T
authors.lastname: Crake
authors.forename: P
authors.initials: P
authors.lastname: Toutouzas
authors.forename: G
authors.initials: G
authors.lastname: Davies
mesh_terms: D001783:Blood Flow Velocity / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D016022:Case-Control Studies; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000378:metabolism* / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005260:Female; D006801:Humans; D007261:Infusions, Intra-Arterial; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000502:physiology; D012965:Sodium Chloride / Q000008:administration & dosage; D018608:Ultrasonography, Doppler; D014664:Vasodilation / Q000502:physiology; D019323:omega-N-Methylarginine / Q000008:administration & dosage
chemical_list: D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D012965:Sodium Chloride