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The Annals of Thoracic Surgery, Vol 54, 1078-1084, Copyright © 1992 by The Society of Thoracic Surgeons
PJ Pearson, PR Evora and HV Schaff
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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Bioassay of EDRF from internal mammary arteries: implications for early and late bypass graft patency
Cardiac Surgical Research, Mayo Clinic, Rochester, Minnesota 55905.
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