Document Detail


The human internal thoracic artery releases more nitric oxide in response to vascular endothelial growth factor than the human saphenous vein.
MedLine Citation:
PMID:  11479503     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Endothelial nitric oxide inhibits smooth muscle cell proliferation, reducing the chance of vascular intimal thickening. In this study we investigated whether the superior long-term patency of the internal thoracic artery in human coronary bypass grafting compared with that of the saphenous vein could be explained by different levels of nitric oxide production. METHODS: The baseline endogenous nitric oxide production appeared to be 50% higher in the internal thoracic artery than in the saphenous vein. Previously, it was shown that vascular endothelial growth factor and the vascular endothelial growth factor receptors KDR (Flk-1) and Flt-1 are expressed in both internal thoracic arteries and saphenous veins and that vascular endothelial growth factor receptor density was higher in internal thoracic arteries than in saphenous veins. Therefore, we also investigated the influence of vascular endothelial growth factor on nitric oxide release in both the internal thoracic artery and the saphenous vein. RESULTS: Vascular endothelial growth factor augmented nitric oxide production by approximately 50% in the saphenous vein and 100% in the internal thoracic artery. As shown by means of immunohistochemistry, expression of endothelial constitutive nitric oxide synthase was similar in the internal thoracic artery and the saphenous vein, and no inducible nitric oxide synthase was expressed in any of the vascular segments. CONCLUSION: Vascular endothelial growth factor augments endothelial constitutive nitric oxide synthase-dependent nitric oxide release to a greater extent in the internal thoracic artery than in the saphenous vein. These findings may help to explain the long-term superiority of the internal thoracic artery versus the saphenous vein as a conduit for coronary artery bypass.
Authors:
M A Broeders; P A Doevendans; J G Maessen; E van Gorsel; M G Egbrink; M J Daemen; G J Tangelder; R S Reneman; R van der Zee
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  122     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-07-31     Completed Date:  2001-09-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  305-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Arginine / pharmacology
Coronary Artery Bypass
Endothelial Growth Factors / pharmacology*
Enzyme Inhibitors / pharmacology
Female
Humans
Immunoenzyme Techniques
Lymphokines / pharmacology*
Male
Middle Aged
Nitric Oxide / metabolism*
Nitric Oxide Synthase / metabolism
Saphenous Vein / metabolism*,  surgery
Thoracic Arteries / metabolism*,  surgery
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Endothelial Growth Factors; 0/Enzyme Inhibitors; 0/Lymphokines; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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