title: Hypoxia increases vasodilator release from internal mammary artery and saphenous vein grafts.
abstract: BACKGROUND
  Greater release of endothelium-derived nitric oxide is implicated in the superior patency of the internal mammary artery (IMA) used in coronary artery bypass grafting. This study compared the release of endothelium-derived nitric oxide into the lumen of the IMA and the saphenous vein under normoxic versus hypoxic conditions.
  
  
  METHODS
  Segments of canine IMA and saphenous vein were perfused in vitro. Vasorelaxant activity was measured as vasodilatation of coronary artery smooth muscle induced by the effluent.
  
  
  RESULTS
  Effluents from the IMA and saphenous vein caused comparable vasodilation of coronary artery smooth muscle. The vasodilatation reversed when perfusion was switched to a prosthetic conduit. Vasodilator activity from the IMA and saphenous vein was attenuated by removing the intima of the grafts or by adding N(G)-monomethyl-L-arginine (10(-4) mol/L) or N(G)-nitro-L-arginine (10(-4) mol/L), two inhibitors of nitric oxide synthesis. Indomethacin attenuated vasorelaxant activity from saphenous vein grafts but not IMA grafts (n = 10). Vasodilator release from the IMA and saphenous vein was augmented by hypoxia. This augmentation was inhibited by indomethacin (n = 10, p < 0.05). Hypoxic augmentation reversed with return to normoxia.
  
  
  CONCLUSIONS
  The release of endothelium-derived nitric oxide and prostacyclin from bypass grafts into the lumen, particularly during hypoxemia, could promote the vasodilation of distal coronary arterial beds, enhancing myocardial perfusion.
authors.affiliation: Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota 55905, USA.
authors.forename: P J
authors.initials: PJ
authors.lastname: Pearson
authors.forename: P R
authors.initials: PR
authors.lastname: Evora
authors.forename: B
authors.initials: B
authors.lastname: Discigil
authors.forename: H V
authors.initials: HV
authors.lastname: Schaff
mesh_terms: D000818:Animals; D001026:Coronary Artery Bypass; D003326:Coronary Circulation; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D011464:Epoprostenol / Q000037:antagonists & inhibitors / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology; D007213:Indomethacin / Q000494:pharmacology; D008323:Mammary Arteries / Q000378:metabolism* / Q000637:transplantation; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D019335:Nitroarginine / Q000494:pharmacology; D010975:Platelet Aggregation Inhibitors / Q000378:metabolism; D012501:Saphenous Vein / Q000378:metabolism* / Q000637:transplantation; D017539:Tunica Intima / Q000378:metabolism; D014654:Vascular Patency; D014664:Vasodilation; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D010975:Platelet Aggregation Inhibitors; D019335:Nitroarginine; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D011464:Epoprostenol; D007213:Indomethacin