ROLE OF NITRIC-OXIDE IN REACTIVE HYPEREMIA IN HUMAN FOREARM VESSELS

Background The role of nitric oxide (NO) in reactive hyperemia (RH) is not well known. We investigated whether NO plays a role in RH in huma n forearm vessels by examining the effects of N-G-monomethyl-L-arginin e (L-NMMA), a blocker of NO synthesis, on reactive hyperemic flow. Met hods and Results Forearm blood flow (FBF) was measured by strain-gauge plethysmography with a venous occlusion technique. The left brachial artery was cannulated for drug infusion and direct measurement of arte rial pressure. To produce RH, blood flow to the forearm was prevented by inflation of a cuff on the upper arm to suprasystolic pressure for intervals of 3 and 10 minutes. After the release of arterial occlusion (AO), FBF was measured every 15 seconds for 3 minutes. Resting FBF wa s 4.31+/-0.3 mL.min(-1) 100 mL(-1) before 3 minutes of AO and 4.1+/-0. 6 mL.min(-1) 100 mL(-1) before 10 minutes of AO. FBF increased to 32.3 +/-1.9 and 38.2+/-3.1 mL.min(-1) 100 mL(-1) immediately after 3 and 10 minutes of AO, respectively, and gradually decayed (n=13). Intra-arte rial infusion of L-NMMA (4 mu mol/min for 5 minutes) decreased baselin e FBF (P<.01) without changes in arterial pressure. L-NMMA did not aff ect the peak reactive hyperemic FBF after 3 and 10 minutes of AO. L-NM MA significantly decreased total reactive hyperemic flow (flow debt re payment) by 20% to 30% after 3 and 10 minutes of AO. Simultaneous infu sion of L-arginine (a precursor of NO) with L-NMMA. reversed the effec ts of L-NMMA. Conclusions Our results suggest that NO plays a minimal role in vasodilation at peak RH but plays a modest yet significant rol e in maintaining vasodilation after peak vasodilation. Our results als o suggest that reactive hyperemia in human forearms is caused largely by mechanisms other than NO.