Nitric oxide maintains dilation of immature and mature collaterals in rat hindlimb.

The role of nitric oxide (NO) in maintaining collateral dilation was investigated in rats with acute and chronic superficial femoral artery occlusion. Collateral function was evaluated from arterial pressure measurements proximal (mean arterial pressure, MAP) and distal (PD) to the occlusion under resting and hyperemic conditions. For resting and hyperemic conditions, respectively, PD increased with the duration of occlusion from 34 +/- 2.1 and 14 +/- 0.8 mm Hg acutely postocclusion to 37 +/- 2.8 and 19 +/- 3.6, 42 +/- 4.9 and 25 +/- 1.5, and 49 +/- 5.6 and 25 +/- 2.1 mm Hg at 1, 4, and 12 weeks. After NO synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME), PD in control limbs increased but in occluded limbs decreased by 20 +/- 2.0 mm Hg (acute) and 18 +/- 2.1, 15 +/- 4.4, and 20 +/- 8.1 mm Hg at 1, 4, and 12 weeks postligation, respectively. The percent of MAP (%MAP) dissipated by large arteries and collateral vessels decreased during collateral development (from 71 +/- 1.7% acutely to 57 +/- 2.2% at 12 weeks postligation) and was increased approximately 20% by L-NAME at each time point. The rise in PD and decrease in %MAP dissipated by collaterals following chronic occlusion indicates that significant collateral development occurred. The fall in PD and increase in %MAP dissipation after L-NAME administration suggest that NO-mediated vasodilatory tone is maintained throughout the period of collateral development.