EXPLANTED VEIN GRAFTS WITH AN INTACT ENDOTHELIUM DEMONSTRATE REDUCED FOCAL EXPRESSION OF ENDOTHELIAL NITRIC OXIDE SYNTHASE SPECIFIC TO ATHEROSCLEROTIC SITES
✍ Scribed by BUTTERY, LEE D. K.; CHESTER, ADRIAN H.; SPRINGALL, DAVID R.; BORLAND, JULIE A. A.; MICHEL, THOMAS; YACOUB, MAGDI H.; POLAK, JULIA M.
- Book ID
- 102646786
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 859 KB
- Volume
- 179
- Category
- Article
- ISSN
- 0022-3417
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✦ Synopsis
The endothelial L-arginine:nitric oxide (NO) system is fundamental to vascular function. It is becoming evident that this system is compromised in aorto-coronary vein grafts, although it is not clear how it is affected. It was postulated that the development of intimal lesions in vein grafts may he associated with reduced expression or loss of endothelial NO synthase (eNOS). The immunocytochemical localization and quantitative expression of eNOS were therefore investigated in normal human saphenous veins (n = 6) and explanted vein grafts (n=6). The vein grafts demonstrated marked morphological changes evident as fihro-intimal hyperplasia (FIH) and focal sites of atherosclerosis, often occurring along the same length of graft. Staining for eNOS was abundantly evident in the endothelium of normal veins hut revealed a differential reduction in staining intensity in vein grafts. Staining intensity measurements revealed a significant reduction (P<O*OOl) in the amount of eNOS present in areas of atherosclerosis as compared with normal veins and areas of vein graft with FIH changes alone. This reduction in the relative quantity of antigen was specific to eNOS, since the endothelial markers von Willehrand factor (vWf) and CD31 showed no such variations. These data support the view that vascular activity of N O is impaired in atherosclerosis and indicate that reduced expression of eNOS, and therefore by inference lower N O production, may make an important contribution to this phenomenon.