Peripheral chemoreflex inhibition with low-dose dopamine: new insight into mechanisms of extreme apnea.
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.
Center for Heart Lung and Vascular Health, University of British Columbia, Kelowna, British Columbia, Canada; Anthony.bain@ubc.ca.
Anthony R
AR
Bain
School of Medicine, University of Split, Split, Croatia;
Zeljko
Z
Dujic
Center for Heart Lung and Vascular Health, University of British Columbia, Kelowna, British Columbia, Canada;
Ryan L
RL
Hoiland
School of Medicine, University of Split, Split, Croatia;
Otto F
OF
Barak
School of Medicine, University of Split, Split, Croatia;
Dennis
D
Madden
School of Kinesiology, University of Zagreb, Zagreb, Croatia;
Ivan
I
Drvis
Cardiff Metropolitan University, Cardiff, United Kingdom;
Mike
M
Stembridge
Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina; and.
David B
DB
MacLeod
Emory University, Atlanta, Georgia.
Douglas M
DM
MacLeod
Center for Heart Lung and Vascular Health, University of British Columbia, Kelowna, British Columbia, Canada;
Philip N
PN
Ainslie
D000328:Adult; D001049:Apnea / Q000503:physiopathology*; D017704:Baroreflex / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects*; D004298:Dopamine / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D000069336:Neurovascular Coupling / Q000187:drug effects; D010100:Oxygen / Q000097:blood*; D012123:Pulmonary Ventilation / Q000187:drug effects; D012720:Severity of Illness Index
D010100:Oxygen; D004298:Dopamine
blood pressure; breath hold; carotid body; cerebral