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

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 NG-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, NG-monomethyl-L-arginine 1 mmol/L and NG-nitro-L-arginine 10 micromol/L attenuated PSD by 57.5% (P<0.001, n=6) and 63.9% (P<0.05, n=6), respectively. Indomethacin 10 micromol/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.