Trans-cerebral HCO3− and PCO2 exchange during acute respiratory acidosis and exercise-induced metabolic acidosis in humans
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO3−]) and carbon dioxide tension (PCO2) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO2 (PaCO2) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO3−] increased by 0.15 ± 0.05 mmol ⋅ l−1 per mmHg elevation in PaCO2 across a wide physiological range (35 to 60 mmHg PaCO2; P < 0.001). The narrowing of the venous-arterial [HCO3−] and PCO2 differences with respiratory acidosis were both related to the hypercapnia-induced elevations in cerebral blood flow (CBF) (both P < 0.001; subset n = 27); thus, trans-cerebral [HCO3−] exchange (CBF × venous-arterial [HCO3−] difference) was reduced indicating a shift from net release toward net uptake of [HCO3−] (P = 0.004). Arterial [HCO3−] was reduced by −0.48 ± 0.15 mmol ⋅ l−1 per nmol ⋅ l−1 increase in arterial [H+] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO3−] difference and arterial [H+] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO3−] exchange was unaltered throughout exercise when indexed against arterial [H+] or pH (P = 0.933 and P = 0.896, respectively). These results indicate that increases and decreases in systemic [HCO3−] – during acute respiratory/exercise-induced metabolic acidosis, respectively – differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO3−] exchange).
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Cerebral Blood Flow and Metabolism |
| Vol/bind | 42 |
| Udgave nummer | 4 |
| Sider (fra-til) | 559-571 |
| Antal sider | 13 |
| ISSN | 0271-678X |
| DOI | |
| Status | Udgivet - 2022 |
| Eksternt udgivet | Ja |
Bibliografisk note
(Ekstern)
Funding Information:
The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Philip N. Ainslie was funded by the Natural Sciences and Engineering Research Council of Canada (NSERC) and a Canada Research Chair. Hannah G. Caldwell was funded by a NSERC PGS-Doctoral Scholarship. Patrice Brassard was funded by the Foundation of the Institut universitaire de cardiologie et de pneumologie de Québec and a NSERC Discovery Grant. Damian M. Bailey was supported by a Royal Society Wolfson Research Fellowship (#WM170007) and Higher Education Funding Council for Wales (Postdoctoral Fellowship for Benjamin S. Stacey). Acknowledgements
Funding Information:
We would like to extend our thanks to the volunteers who participated in these studies. Additionally, we would like to thank past and present members of the Centre for Heart, Lung and Vascular Health at UBCO for their contribution to this series of studies by our group. The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Philip N. Ainslie was funded by the Natural Sciences and Engineering Research Council of Canada (NSERC) and a Canada Research Chair. Hannah G. Caldwell was funded by a NSERC PGS-Doctoral Scholarship. Patrice Brassard was funded by the Foundation of the Institut universitaire de cardiologie et de pneumologie de Qu?bec and a NSERC Discovery Grant. Damian M. Bailey was supported by a Royal Society Wolfson Research Fellowship (#WM170007) and Higher Education Funding Council for Wales (Postdoctoral Fellowship for Benjamin S. Stacey).
Publisher Copyright:
© The Author(s) 2021.
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