This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Calvo, W. J. Articles by Diamond, S. L. Search for Related Content PubMed PubMed Citation Articles by Calvo, W. J. Articles by Diamond, S. L. Related Collections Endothelium/vascular type/nitric oxide

(Circulation. 1999;99:1069-1076.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Inhibition of Nitric Oxide but Not Prostacyclin Prevents Poststenotic Dilatation in Rabbit Femoral Artery

William J. Calvo, PhD; George Hajduczok, PhD; James A. Russell, PhD; Scott L. Diamond, PhD

From the Bioengineering Laboratory, Department of Chemical Engineering (W.J.C.), and the Department of Physiology and Biophysics, School of Medicine (G.H., J.A.R.), State University of New York at Buffalo, and the Institute for Medicine and Engineering, Department of Chemical Engineering, University of Pennsylvania, Philadelphia, Pa (S.L.D.).

Correspondence to Scott L. Diamond, Institute for Medicine and Engineering, Department of Chemical Engineering, 394 Towne Bldg, University of Pennsylvania, Philadelphia, PA 19104. E-mail sld{at}eniac.seas.upenn.edu

Background—Poststenotic dilatation (PSD) occurs in a low-pressure region where recirculation eddies oscillate in size during the cardiac cycle. NO may be an important mediator of PSD.

Methods and Results—Femoral arteries of 7 adult male New Zealand White rabbits were stenosed bilaterally to achieve a diameter reduction of 70.9±6.7% (n=14). At the time of stenosis, the adventitia of one of the arteries was coated with 1 mmol/L of N^G-nitro-L-arginine methyl ester (L-NAME) in 22% (wt/vol) Pluronic gel, while the contralateral vessel was coated with gel without L-NAME. In stenosed femoral arteries that were treated with gel without L-NAME, a maximum PSD of 30.99±7.92% (n=7) was observed in polymer casts at 3 days relative to the mean proximal diameter of 1.57±0.25 mm at a position 12 mm upstream of each stenosis. In contrast, the vessels treated with L-NAME exhibited a maximum PSD of only 7.16±8.81% (n=7) relative to the mean proximal diameter of 1.55±0.16 mm. L-NAME caused a 76.9% reduction (P<0.001, n=7) of PSD. Similarly, N^G-monomethyl-L-arginine 1 mmol/L and N^G-nitro-L-arginine 10 µmol/L attenuated PSD by 57.5% (P<0.001, n=6) and 63.9% (P<0.05, n=6), respectively. Indomethacin 10 µmol/L caused no reduction in PSD. Arterial rings obtained from the poststenotic region were more sensitive and responsive to acetylcholine than those obtained proximal to the stenosis.

Conclusions—NO, but not prostacyclin, is a major mediator of PSD.

Key Words: endothelium • hemodynamics • stenosis

This article has been cited by other articles:

				S. S. Meyrelles, R. V. Sharma, H. Z. Mao, F. M. Abboud, and M. W. Chapleau Modulation of baroreceptor activity by gene transfer of nitric oxide synthase to carotid sinus adventitia Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2003; 284(5): R1190 - R1198. [Abstract] [Full Text] [PDF]

				A. Maiorana, G. O'Driscoll, L. Dembo, C. Cheetham, C. Goodman, R. Taylor, and D. Green Effect of aerobic and resistance exercise training on vascular function in heart failure Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1999 - H2005. [Abstract] [Full Text] [PDF]