Supplemental oxygen does not modulate responses to acetylcholine or ascorbic acid in the forearm of patients with congestive heart failure

Despite providing symptomatic relief in patients with congestive heart failure (CHF), supplemental oxygen (O₂) has been demonstrated to increase total peripheral resistance. The present study investigated the possibility that O₂ inhalation reduces nitric oxide (NO) bioavailability, using endothelium-dependent (acetylcholine) and -independent (phentolamine) vasodilators, and the antioxidant ascorbic acid. Ten patients (nine male and one female) with primary left ventricular failure participated in the study. Forearm venous occlusion plethysmography was used to study blood flow responses to acetylcholine and the α-adrenergic antagonist phentolamine during inhalation of either room air or 100% O₂, with and without the simultaneous infusion of ascorbic acid. Neither O₂ inhalation (3.9±0.4 compared with 3.8±0.3 ml⋅min^-1⋅100 ml^-1) nor ascorbic acid infusion (5.2±0.4 compared with 5.5±0.4 ml⋅min^-1⋅100 ml^-1) affected resting forearm blood flow. The percentage increase from basal blood flow after acetylcholine infusion was not altered by either O₂ inhalation or ascorbic acid infusion (room air, 140±55%; O₂, 118±46%; ascorbic acid, 147±39%; ascorbic acid+O₂, 109±31%). O₂ inhalation did, however, reduce the dilation induced by phentolamine (room air, 131±24%; O₂, 80±14%; P < 0.05). These data indicate that oxygen inhalation does not increase forearm vascular resistance. Secondly, preservation of reactivity to acetylcholine during O₂ inhalation suggests that degradation of NO by O₂-derived free radicals is not enhanced. Attenuation of phentolamine-induced vasodilation during O₂ inhalation, however, implies increased adrenergic activity, which may possibly exacerbate the detrimental effects of elevated sympathetic activity in CHF.