Hyperoxia inhibits production of endothelial nitric oxide in humans
(English)Manuscript (preprint) (Other academic)
Hypceoxia causes vasoconstriction in most tissues, but the mechanisms have yet to be elucidated. One hypothesis is that hyperoxia affects the production of free oxygen radicals (ROS), which reduce the concentration of the vasorelaxing agent nitric oxide (NO). It is not clear whether ROS reduce the synthesis of NO or inactivate NO that is already present. We investigated the effects of breathing 100% oxygen on NO-mediated vasodilation. Iontophoresis was used to deliver acetylcholine (ACh) (which stimulates endothelium-dependent production of NO) and sodium nitroprusside (SNP) (a NO-donor) through the skin of healthy volunteers (n=9). The blood flow in the skin was measured with a laser Doppler perfusion imager and dose-response curves were plotted. The drug dose at which 50% of the total perfusion increase was reached was calculated (ED50). The ED50 was significantly higher (right-shifted curve) while breathing oxygen compared with breathing air, when ACh was given by iontophoresis (95% CI 0.26 to 2.2). When ACh iontophoresis was preceded by oral intake of vitamin C (2.5 g daily for 3 days), this effect was abolished. Hyperoxla had no effect on vasodilation after iontophoresis with SNP. These results favour the hypothesis that hyperoxic vasoconstriction is mediated through inhibition of synthesis of NO by free oxygen radicals inside the endothelial cells.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-83825OAI: oai:DiVA.org:liu-83825DiVA: diva2:558221