title: The role of endogenous nitric oxide in the response of coronary blood flow to tachycardia.
abstract: BACKGROUND
  The role of endogenous nitric oxide as mediator of flow-dependent dilation is well established. However, its role in the adaptation of coronary blood flow to tachycardia is less well defined. This study was designed to determine whether nitric oxide is a mediator in pacing-induced hyperaemia.
  
  
  METHODS
  Twenty pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing measurements. Their heart rate was increased by 20 beats every 5 min. Coronary blood flow was measured basally and at each pacing interval before and after each of the following interventions: intracoronary saline infusion (n = 6), N omega-nitro-L-arginine methyl ester infusion (L-NAME, 20 micrograms/kg per min intracoronarily, n = 9) and infusion of L-NAME plus L-arginine (0.3 mg/kg per min intracoronarily, n = 5).
  
  
  RESULTS
  The coronary peak flow increased with atrial pacing. The maximum increase in coronary blood flow with pacing was significantly reduced after infusion of L-NAME (159 +/- 33 versus 143 +/- 30%), whereas no change was observed in the saline group (163 +/- 28 versus 172 +/- 29%). However, it increased significantly in the group receiving L-NAME plus L-arginine (147 +/- 29 versus 182 +/- 40%).
  
  
  CONCLUSIONS
  In the pig, the increase in coronary blood flow and therefore the vasodilation of the microvasculature that accompanies tachycardia depend, partly, on the release of endogenous nitric oxide.
authors.affiliation: Cardiovascular Research Unit, Hospital Clinic i Provincial, University of Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Heras
authors.forename: E
authors.initials: E
authors.lastname: Roig
authors.forename: F
authors.initials: F
authors.lastname: Pérez-Villa
authors.forename: M
authors.initials: M
authors.lastname: Paz
authors.forename: G
authors.initials: G
authors.lastname: Melis
authors.forename: M
authors.initials: M
authors.lastname: Rigol
authors.forename: F
authors.initials: F
authors.lastname: Epelde
authors.forename: G
authors.initials: G
authors.lastname: de Candia
authors.forename: G
authors.initials: G
authors.lastname: Sanz
mesh_terms: D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004338:Drug Combinations; D004730:Endothelium, Vascular / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007261:Infusions, Intra-Arterial; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D013552:Swine; D013610:Tachycardia / Q000503:physiopathology* / Q000628:therapy; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D004338:Drug Combinations; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester