title: Effect of ascorbic acid on endothelium-dependent vasodilatation of human arterial conduits for coronary artery bypass grafting.
abstract: OBJECTIVE
  Techniques aimed at improving the performance of arterial conduits will maximize the clinical benefit achievable with coronary artery bypass surgery. Controlling oxidant stress could be a strategy for preventing early graft deterioration. We tested the effect of a free radical scavenger, ascorbic acid (vitamin C), on preserving the endothelium-dependent vasodilatation function in vitro of radial artery and internal thoracic artery. We also tested its effect on the amount of reactive oxygen species (ROS) generated by each graft.
  
  
  METHODS
  Radial artery (RA, n=25) and internal thoracic (ITA, n=19) segments were obtained from coronary artery bypass grafting patients. Each segment was divided into 3-4 mm vascular rings and incubated with or without ascorbic acid (10(-3) mol/l) for 1 h or 72 h. Using the organ bath technique, the endothelium-dependent vasodilatation function was tested in vitro by the addition of cumulative concentrations of acetylcholine (10(-9)-10(-5) mol/l) following vasocontraction by endothelin-1 (3 x 10(-8) mol/l). ROS were measured by using chemiluminescence technique at 1-h and after 72 h incubation with or without ascorbic acid.
  
  
  RESULTS
  There were no differences in the vasodilatation function between control and ascorbic acid group of both arteries in the 1-hour incubation experiment. However, in the 72 h incubation experiment, ascorbic acid preserved the endothelium-dependent vasodilatation function of RA compared with control group (35.8+/-2.2% vs. 25.9+/-2.1%; P=0.005), but not ITA (39+/-3.5% vs. 40.5+/-9.3%; P=0.438). After 72 h incubation, RA generated significantly more free radicals compared with 1 h (133.7+/-151.5 vs. 16.8+/-16.8 cps/mg x 100; P=0.01); however, AA has no statistically significant effect on decreasing the amount of free radicals generated by both arteries.
  
  
  CONCLUSIONS
  In RA, ascorbic acid is able to preserve the endothelium-dependent vasodilatation function after 72 h incubation, but not after 1 h. However, the mechanism of action of AA is not completely understood. This finding could open the door for understanding the role of oxidant stress and antioxidants in preserving the endothelial function of coronary artery bypass grafts.
mesh_terms: D000368:Aged; D001205:Ascorbic Acid / Q000494:pharmacology*; D001026:Coronary Artery Bypass; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008323:Mammary Arteries / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D008875:Middle Aged; D009924:Organ Culture Techniques; D018384:Oxidative Stress / Q000187:drug effects; D017534:Radial Artery / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D013481:Superoxides / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D013481:Superoxides; D001205:Ascorbic Acid