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  • Title: Hypoxia increases vasodilator release from internal mammary artery and saphenous vein grafts.
    Author: Pearson PJ, Evora PR, Discigil B, Schaff HV.
    Journal: Ann Thorac Surg; 1998 May; 65(5):1220-5. PubMed ID: 9594841.
    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.
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