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The Influence of Carbon Monoxide on Vascular Reactivity
- Author / Creator
- Thrall, Scott
Background: Carbon monoxide alters cardiovascular function through its actions as a signaling molecule and by limiting oxygen delivery in the blood, favouring pro-dilatory and anti-constrictor effects within the vasculature. The impacts of mild carbon monoxide exposure on vascular responses to exercise and sympathetic vasoconstriction have not been previously assessed in humans. We hypothesized that mild increases in circulating carbon monoxide would increase the magnitude of vasodilation in response to exercise, and inhibit α1 adrenergic vasoconstriction.
Methods: Cardiovascular function was assessed via measurement of heart rate (ECG), mean arterial pressure (finger plethysmography), brachial artery diameter (B-mode ultrasound), forearm blood flow (FBF) (duplex ultrasound) and vascular conductance (FVC) (calculated from mean arterial pressure and FBF) in 19 young healthy volunteers (10 females) before and after carbon monoxide inhalation, and compared against a second control day without carbon monoxide exposure in a randomized control trial design. Measures were collected during resting baseline, rhythmic handgrip exercise (15% of maximum voluntary contraction) to assess the vascular response to exercise, and during continued exercise following a venous bolus infusion of the α1 adrenergic agonist phenylephrine to assess sympathomimetic vasoconstriction. The magnitude of vasoconstriction during the initial peak constrictor response and between 90- and 120-seconds post-infusion were quantified as indices of α1 adrenergic sensitivity. Forearm vascular data were obtained in both the exercising and resting arms to investigate the effects of carbon monoxide in both working and inactive tissue.
Results: Handgrip exercise elicited mild increases in heart rate (P<0.05), and substantial increases in FBF and FVC in the exercising arm (P<0.05). Phenylephrine infusion elicited decreases in heart rate (P<0.05), increases in mean arterial pressure (P<0.05), and reductions in FBF and FVC in both the exercising and resting arms (P<0.05). Carbon monoxide inhalation increased circulating carboxyhemoglobin saturation to 5.6 ± 1.2%. No differences in cardiovascular responses were detected with carbon monoxide exposure, either in relative (percent change) or absolute measures.
Conclusions and Significance: Our data indicate that mild carbon monoxide does not alter functional vascular reactivity to exercise nor to α1 adrenergic stimulation. These findings conflict with previous works demonstrating greater vasodilation with higher levels of exposure and attenuated vasoconstriction in isolated models, suggesting that alternate compensatory mechanisms abolish these effects at the present level of carbon monoxide exposure in humans. These findings improve our understanding of vascular function during moderate perturbations in vasoactive signaling, and support that mild carbon monoxide exposure does not constitute a significant threat to vascular regulation and oxygen delivery during physical activity.
- Graduation date
- Spring 2022
- Type of Item
- Master of Science
- 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.