The Impact of Carbon Monoxide on Endothelial Function

• Author / Creator

  Cheung, Nicholas

• 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.

• Subjects / Keywords

  • Endothelial Function
  • Flow Mediated dilation
  • vascular physiology
  • carbon monoxide

• Graduation date

  Fall 2023

• Type of Item

  Thesis

• Degree

  Master of Science

• DOI

  https://doi.org/10.7939/r3-36kq-9x43

• License

  This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.