Effects of supplemental oxygen on forearm vasodilation in humans

Abstract

Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 +/- 7.9 vs. 47.8 +/- 6.7 ml.min-1.100 ml-1; P < 0.02; vascular resistance 1.7 +/- 0.2 vs. 2.4 +/- 0.4 mmHg.min.100 ml.ml-1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; -30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2 raised minimal resistance (2.3 +/- 0.4 RA; 2.8 +/- 0.5 O2+LBNP+VC, P < 0.04). When O2 alone (experiment 1) was compared with O2+LBNP+VC (experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

Vitamin C prevents hyperoxia-mediated vasoconstriction and impairment of endothelium-dependent vasodilation

“…The observation that hyperoxia increased vascular resistance in both groups is consistent with the findings of many investigators (2,4,6,7,11,23,28). We have made the novel observation that hyperoxic vasoconstriction is prevented by vitamin C, suggesting that hyperoxia-associated ROS are mediators of this vascular response.…”

“…Release of NO from these compounds is likely inversely related to blood O 2 tension (15). Vitamin C may thus prevent hyperoxic vasoconstriction by several mechanisms involving NO bioavailability, including direct quenching of superoxide anions, stabilization of BH 4 , and possibly increasing the release of NO from peroxynitrite and nitrosylated compounds (24).…”

“…Moreover, hyperoxia impairs acetylcholine-mediated vasodilation in the setting of intact endothelial function. These effects of hyperoxia are prevented by vitamin C, providing evidence that hyperoxia-derived free radicals impair the activity of endotheliumderived vasoactive factors.oxygen; acetylcholine; heart failure; endothelium HIGH ARTERIAL BLOOD OXYGEN (O 2 tension) causes vasoconstriction in healthy humans (2,4,6,7,28). Although hyperoxic vasoconstriction was first reported at least 90 years ago (2), the mechanism(s) for this phenomenon in healthy humans is poorly understood.…”

“…oxygen; acetylcholine; heart failure; endothelium HIGH ARTERIAL BLOOD OXYGEN (O 2 tension) causes vasoconstriction in healthy humans (2,4,6,7,28). Although hyperoxic vasoconstriction was first reported at least 90 years ago (2), the mechanism(s) for this phenomenon in healthy humans is poorly understood.…”

Hyperoxia Attenuates Endothelial-Mediated Vasodilation in the Human Skin

“…An understanding of hyperoxic effects on the circulatory system is fundamental to the understanding of the efficacy of hyperbaric oxygen therapy in clinical situations, though the effect of hyperoxia on the skin circulation is still unclear. It has been reported that supplemental oxygen increases peripheral vascular resistance [1,2] and decreases the limb vasodilator response to forearm ischemia [3]. Since the sympathetic nerve activity to muscle is decreased or unchanged under hyperoxic conditions [4,5], this peripheral vasoconstriction may be associated with nonsympathetic mechanisms.…”