Peripheral chemoreflex inhibition with low-dose dopamine: New insight into mechanisms of extreme apnea
Author
Bain, Anthony
Dujic, Zeljko
Hoiland, Ryan
Barak, Otto
Madden, Dennis
Drvis, Ivan
Stembridge, Mike
Macleod, David
Ainslie, Phillip
Date
2015-11-01Acceptance date
2015-08-11
Type
Article
Publisher
American Physiological Association
ISSN
1522-1490
Metadata
Show full item recordAbstract
The purpose of this study was to determine the impact of peripheral chemoreflex inhibition with low-dose dopamine on maximal apnea time, and the related hemodynamic and cerebrovascular responses in elite apnea divers. In a randomized order, participants performed a maximal apnea while receiving either intravenous 2 μg·kg−1·min−1 dopamine or volume-matched saline (placebo). The chemoreflex and hemodynamic response to dopamine was also assessed during hypoxia [arterial O2 tension, (PaO2) ∼35 mmHg] and mild hypercapnia [arterial CO2 tension (PaCO2) ∼46 mmHg] that mimicked the latter parts of apnea. Outcome measures included apnea duration, arterial blood gases (radial), heart rate (HR, ECG), mean arterial pressure (MAP, intra-arterial), middle (MCAv) and posterior (PCAv) cerebral artery blood velocity (transcranial ultrasound), internal carotid (ICA) and vertebral (VA) artery blood flow (ultrasound), and the chemoreflex responses. Although dopamine depressed the ventilatory response by 27 ± 41% (vs. placebo; P = 0.01), the maximal apnea duration was increased by only 5 ± 8% (P = 0.02). The PaCO2 and PaO2 at apnea breakpoint were similar (P > 0.05). When compared with placebo, dopamine increased HR and decreased MAP during both apnea and chemoreflex test (P all <0.05). At rest, dopamine compared with placebo dilated the ICA (3.0 ± 4.1%, P = 0.05) and VA (6.6 ± 5.0%, P < 0.01). During apnea and chemoreflex test, conductance of the cerebral vessels (ICA, VA, MCAv, PCAv) was increased with dopamine; however, flow (ICA and VA) was similar. At least in elite apnea divers, the small increase in apnea time and similar PaO2 at breakpoint (∼31 mmHg) suggest the apnea breakpoint is more related to PaO2, rather than peripheral chemoreflex drive to breathe.
Journal/conference proceeding
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology;
Citation
Bain, A.R., Dujic, Z., Hoiland, R.L., Barak, O.F., Madden, D., Drvis, I., Stembridge, M., MacLeod, D.B., MacLeod, D.M. and Ainslie, P.N. (2015) 'Peripheral chemoreflex inhibition with low-dose dopamine: new insight into mechanisms of extreme apnea', American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 309(9), pp.R1162-R1171. DOI: 10.1152/ajpregu.00271.2015.
Description
Article published in American Journal of Physiology - Regulatory, Integrative and Comparative Physiology on 01 November 2015, freely available at: https://doi.org/10.1152/ajpregu.00271.2015.
Sponsorship
Cardiff Metropolitan University (Grant ID: Cardiff Metropolian (Internal))
Canadian Research Chair and Natural Sciences and Engineering Research Council (NSERC) Discovery grant held by P. N. Ainslie. Z. Dujic, O. F. Barak, and P. N. Ainslie were also funded through the Croatian Science Foundation. A. R. Bain was funded through a postgraduate NSERC scholarship.
Collections
- Sport Research Groups [1088]
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