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 lowdose 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.