DIRECT IN-VIVO MEASUREMENT OF FLOW-DEPENDENT NITRIC-OXIDE PRODUCTION IN MESENTERIC RESISTANCE ARTERIES

Purpose: To determine whether the concentration of nitric oxide (NO) a t the arterial wall is increased subsequent to the abrupt elevation of blood now in resistance arteries. Methods: Eight dogs underwent lapar otomy with anesthesia, and their small bowels were exteriorized. NO co ncentration was measured with NO-specific electrodes (200-mu-tip diame ter) at the outer wall of the mesenteric arteries. Flow was increased by occlusion of the adjacent mesenteric arteries. In four animals, flo w and NO concentration were measured after the administration of N ome ga-nitro-L-arginine-methyl ester (L-NAME) to inhibit NO production. Re sults: As arterial flow was increased from a baseline of 5.4 +/- 1.3 m l/min to 10.9 +/- 1.8 ml/min (p = 0.001), NO electrode current was ele vated in every animal. With repetition of the flow stimulus, the respo nse tended to be attenuated. In the first experimental trial, NO elect rode current measured at the arterial wall increased from 2.86 +/- 0.5 6 to 3.00 +/- 0.60 nA (p = 0.02). L-NAME (10 mg/kg intravenous) effect ively inhibited NO synthase as indicated by the elevation of mean arte rial pressure (11 +/- 1.7 mm Hg; p = 0.04). After administration of L- NAME, NO electrode current measured at the outer arterial wall fell 0. 23 +/- 0.05 nA (p = 0.02). Conclusions: The data indicate that a doubl ing of blood now in the canine mesenteric resistance arteries is assoc iated with an increase in NO concentration of at least 100 nm at the o uter arterial wall. This association is probably a substantial underes timation of the actual concentration because of the geometry of the el ectrode tip. To our knowledge, ours is the first report of direct in v ivo measurement of now-dependent NO release in resistance arteries.