Inhibition of nitric oxide but not prostacyclin prevents poststenotic dilatation in rabbit femoral artery.

Abstract

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