ACUTE COMPENSATION TO ABRUPT OCCLUSION OF RAT FEMORAL-ARTERY IS PREVENTED BY NO SYNTHASE INHIBITORS

The hemodynamic significance of endothelium-derived relaxing factor (E DRF)-mediated mechanisms in vascular responses to abrupt rat femoral a rtery occlusion was investigated. Temporary arterial occlusion was pro duced before and after inhibition of nitric oxide synthase by N-omega- nitro-L-arginine methyl ester (L-NAME) or N-G-monomethyl-L-arginine (L -NMMA). Iliac artery blood flow and arterial pressures proximal and di stal to the occlusion were measured. Normal vascular compensation incl uded a return of resistance to preocclusion levels and a rise in dista l pressure to a plateau within 5 min postocclusion. After treatment wi th L-NAME and L-NMMA, postocclusion resistance remained elevated by 53 and 36%, respectively. Collateral dilation after occlusion, as indica ted by the rise in distal pressure, was prevented by L-NAME but not L- NMMA. Increases in adrenergic tone and mean arterial pressure by pheny lephrine did not prevent compensation, suggesting the effects of L-NAM E and L-NMMA did not result from elevated sympathetic activation or pr essure. The results are consistent with the hypothesis that the stimul ated release of endothelium-derived relaxing factor mediates the acute vascular compensation to abrupt arterial occlusion.