The Impact of Carbon Monoxide on Endothelial Function

Abstract

Endothelial function measured via flow-mediated dilation following mild, acute carbon monoxide (CO) exposure was quantified in 19 healthy young non-smoking adult participants (n=10 females). The Schmidt-Prommer rebreathe method for the measurement of blood volume was used for the CO exposure, and standardized flow-mediated dilation techniques were utilized. It was hypothesized that CO would increase endothelial-dependent vasodilation in vascular smooth muscle, potentially by modulation of endothelial nitric oxide synthase, intracellular NO release, or the dilatory cGMP pathway. While carboxyhemoglobin (COHb%) was elevated following the rebreathe (5.64±1.24%), mean arterial pressure, heart rate, blood flow, brachial artery diameter, and forearm vascular conduction were not significantly different following the CO rebreathe protocol. FMD and FMD%, as well as shear corrected FMD:ssAUC and FMD%:ssAUC were also not significantly different following CO rebreathe. These results suggest mildly elevated COHb% does not impact resting vascular and hemodynamic parameters, or impact endothelial-dependent vasodilation. Further research exploring CO release from hemoglobin to tissue could provide insight into endothelial cell exposure of CO following mild, acute exposure.