ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Paul J. Pearson
Berent Discigil
Hartzell V. Schaff
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pearson, P. J.
Right arrow Articles by Schaff, H. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pearson, P. J.
Right arrow Articles by Schaff, H. V.

Ann Thorac Surg 1998;65:1220-1225
© 1998 The Society of Thoracic Surgeons

Hypoxia Increases Vasodilator Release From Internal Mammary Artery and Saphenous Vein Grafts

Paul J. Pearson, MD, PhDa, Paulo R.B. Evora, MD, PhDa, Berent Discigil, MDa, Hartzell V. Schaff, MDa

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.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1998 by The Society of Thoracic Surgeons.