Hemodynamic and biochemical effects of 100% oxygen breathing in humans

Abstract

High concentrations of inspired oxygen have been reported to have significant hemodynamic effects that may be related to increased free radical production. If oxygen therapy increases free radical production, it may also modify hemodynamic responses to a nitric oxide donor. Twenty-nine healthy male volunteers were studied using randomized, double-blind, placebo-controlled, crossover designs to determine whether oxygen therapy is associated with hemodynamic and forearm vascular effects. We measured hemodynamic parameters and forearm vascular responses before and 1 h after exposure to 100% oxygen versus medical air. Plasma 8-iso-PGF2alpha and plasma vitamin C were measured to assess the biochemical effects of oxygen administration. Hemodynamic measurements were also made following the acute administration of sublingual nitroglycerin. Oxygen therapy caused no significant change in blood pressure, plasma 8-iso-PGF2alpha, or vitamin C. Oxygen did cause a significant reduction in heart rate and forearm blood flow, and an increase in peripheral vascular resistance. Oxygen caused no change in the hemodynamic response to nitroglycerin. Therefore, in healthy young adults, therapy with 100% oxygen does not affect blood pressure, despite causing an increase in vascular resistance, is not associated with evidence of increased free radical injury, and does not affect the hemodynamic responses to nitroglycerin.

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.…”

“…The three conditions were separated by at least 12 min to reestablish the baseline state. This protocol was not performed in healthy volunteers, because in this population, a vasoconstrictor effect of hyperoxia persisting Ͼ1 h has been previously demonstrated in our laboratory (28).…”

“…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.…”

WHO Needs High FIO2?

“…In the lung it has been observed decreased mucociliar transport, inflammatory reaction, focal pulmonary edema, interstitial fibrosis and reabsorption atelectasis. In the cardiocirculatory system, higher oxygen tension decreases cardiac output and stroke volume with increased peripheral vascular resistances and coronary artery vasoconstriction (66)(67)(68)(69). The peripheral vasoconstriction, in particular, may explain the possible gap between high PaO 2 and low tissue oxygen tension.…”