NITRIC-OXIDE MAINTAINS DILATION OF IMMATURE AND MATURE COLLATERALS INRAT HINDLIMB

The role of nitric oxide (NO) in maintaining collateral dilation was i nvestigated in rats with acute and chronic superficial femoral artery occlusion. Collateral function was evaluated from arterial pressure me asurements proximal (mean arterial pressure, MAP) and distal (P-D) to the occlusion under resting and hyperemic conditions. For resting and hyperemic conditions, respectively, P-D 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 inhibi tion with No-nitro-L-arginine methyl ester (L-NAME), P-D in control li mbs increased but in occluded limbs decreased by 20 +/- 2.0 mm Hg (acu te) and 18 +/- 2.1, 15 +/- 4.4, and 20 +/- 8.1 mm Hg at 1, 4, and 12 w eeks postligation, respectively. The percent of MAP (%MAP) dissipated by large arteries and collateral vessels decreased during collateral d evelopment (from 71 +/- 1.7% acutely to 57 +/- 2.2% at 12 weeks postli gation) and was increased similar to 20% by L-NAME at each time point. The rise in P-D and decrease in %MAP dissipated by collaterals follow ing chronic occlusion indicates that significant collateral developmen t occurred. The fall in P-D and increase in %MAP dissipation after L-N AME administration suggest that NO-mediated vasodilatory tone is maint ained throughout the period of collateral development.