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Ann Thorac Surg 1992;54:1078-1084
© 1992 The Society of Thoracic Surgeons
Cardiac Surgical Research and Section of Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
* Address reprint requests to Dr Schaff, Section of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
To study the basal, luminal release of endothelium-derived relaxing factor, 35-mm segments of canine internal mammary artery (IMA) were cannulated and perfused at 5 mL/min in vitro with physiological salt solution. Vasoactive properties of the effluent were bioassayed on coronary artery smooth muscle. Effluent from IMAs produced significant vasodilation of the bioassay ring compared with effluent from a prosthetic conduit (n = 24; p < 0.05). The vasodilation by the effluent could be eliminated by mechanically removing the intima of the IMA, or by treating the IMA segments with NG-monomethyl-L-arginine or NG-nitro-L-arginine, two competitive inhibitors of nitric oxide synthesis from L-arginine; vasodilation was not influenced by treatment with indomethacin. In 83% of the superfusion experiments, effluent from the left IMA induced greater relaxation of the bioassay ring than did effluent from the right IMA. In addition, the average vasodilation induced by left IMA effluent was 28% ± 2.3% versus 17.4% ± 3.1% for the right (n = 24; p < 0.05). However, in organ chamber experiments, right and left IMAs exhibited comparable endothelium-dependent vasodilation to acetylcholine (n = 6). Because endothelium-derived relaxing factor induces vasodilation and also inhibits platelet adhesion, platelet aggregation, and atherogenesis, luminal release of endothelium-derived relaxing factor by the IMA could contribute to superior results when the artery is used in bypass grafting.
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