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 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-Larginine 10 mu mol/L attenuated PSD by 57.5% (P<0.001, n=6) and 63.9% (P<0.05, n=6), respectively. Indomethacin 10 mu mol/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, Conclusion-NO, but not prostacyclin, is a major mediator of PSD.