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 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 min. 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.