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Ann Thorac Surg 1998;65:1220-1225
© 1998 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
Accepted for publication November 26, 1997.
Address reprint requests to Dr Schaff, Mayo Clinic, 200 First St SW, Rochester, MN 55905
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 vasodilatation 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 NG-monomethyl-L-arginine (10-4 mol/L) or NG-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 vasodilatation of distal coronary arterial beds, enhancing myocardial perfusion.
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