We hypothesized that nitric oxide (NO) elicited by high fluid shear stress acting on the endothelium in the throat of the stenosis and/or at the focal site of flow reattachment may be an important mediator of poststenotic dilatation (PSD). Femoral arteries of 5 adult male New Zealand white rabbits were stenosed bilaterally to achieve a diameter reduction of 74±5% (n=10). At the time of stenosis, the adventitia of a the stenosed arteries was coated with 1 mM of NG-nitro-L-arginine methyl ester (LNAME) in 22% (w/v) pluronic gel, while the contralateral vessel was coated with gel without LNAME. In stenosed femoral arteries that were treated with gel only, a maximum PSD of 29±8% (n=5) was observed in polymer casts at 3 days. In contrast, the vessels treated with LNAME exhibited a maximum PSD of only 4±5% (n=5). Vascular rings from stenosed proximal (n=9) and distal (n=8) segments, as well as from the contralateral sham operated (n=6) arteries were also studied from 3 animals in tissue baths. Endothelium-dependent relaxations to acetylcholine in arteries contracted submaximally by phenylephrine were greater in the distal (PSD) segments (p<0.05) as compared with control or the proximal segments. We conclude that wall shear stresses within the stenosis and/or at the focal site of flow reattachment elicit endothelial production of NO to cause PSD and enhances receptor stimulated release of NO.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology