CHANGES IN PULMONARY VASCULAR TONE DURING EXERCISE - EFFECTS OF NITRIC-OXIDE (NO) SYNTHASE INHIBITION, L-ARGININE INFUSION, AND NO INHALATION

Citation
T. Koizumi et al., CHANGES IN PULMONARY VASCULAR TONE DURING EXERCISE - EFFECTS OF NITRIC-OXIDE (NO) SYNTHASE INHIBITION, L-ARGININE INFUSION, AND NO INHALATION, The Journal of clinical investigation, 94(6), 1994, pp. 2275-2282
Citations number
32
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
0021-9738
Volume
94
Issue
6
Year of publication
1994
Pages
2275 - 2282
Database
ISI
SICI code
0021-9738(1994)94:6<2275:CIPVTD>2.0.ZU;2-1
Abstract
Nitric oxide (NO) is a potent endogenous vasodilator. Its role in the normal and stressed pulmonary circulation is unclear. To better unders tand the importance of endogenous NO in normal physiological responses , we studied the effects of altered NO availability on the change in p ulmonary vascular tone that accompanies exercise. In paired studies we measured blood flow and pressures in the pulmonary circulation at res t and during treadmill exercise at a speed of 4 mph with and without ( a) N omega-nitro-L-arginine, 20 mg/kg intravenously, a selective inhib itor of NO synthase; (b) L-arginine, 200 mg/kg intravenously, substrat e for NO synthase; (c) combination of the inhibitor and substrate; and (d) inhalation of NO > 30 ppm, to determine if endogenous release of NO elicits maximal vasodilation. In addition, we sought to determine t he site of NO effect in the pulmonary circulation by preconstriction w ith either U44619 or hypoxia (fraction of inspired O-2 = 0.12) using a distal wedged pulmonary catheter technique. NO synthase inhibition ra ised pulmonary vascular tone equally at rest and exercise. L-Arginine reversed the effects of NO synthase inhibition but had no independent effect. NO inhalation did not reduce pulmonary vascular tone at rest o r enhance the usual reduction in pulmonary vascular resistance with ex ercise. The effect of NO synthase inhibition was in pulmonary vessels upstream from small veins, suggesting that endogenous NO dilates prima rily small arteries and veins at rest. We conclude that, in sheep, end ogenous NO has a basal vasodilator function that persists during, but is not enhanced by, exercise.