Why the study?
Does hyperoxia reduce muscle sympathetic nerve activity following exposure to hypoxia in humans?
Does hyperoxia reduce muscle sympathetic nerve activity following exposure to hypoxia in humans?
Hyperoxia transiently attenuates the sustained elevation in muscle sympathetic nerve activity following hypoxia, suggesting carotid chemoreceptor input is obligatory for this chemoreflex response.
Hyperoxia may transiently suppress post-hypoxic MSNA via carotid body inhibition; leaves open therapeutic relevance pending controlled trials.
Hypoxia may sensitize the carotid chemoreceptors resulting in a sustained elevation of muscle sympathetic nerve activity (MSNA) which outlasts the hypoxic stimulus. To test this hypothesis we determined (n=4) the effect of carotid body deactivation on the sustained elevation in MSNA (common peroneal nerve) following isocapnic hypoxia (arterial O 2 saturation 80% for 20 mins) in humans. Ventilation, heart rate and MSNA were elevated in hypoxia; however, only the elevation in MSNA outlasted the hypoxic stimulus, and remained elevated for 20 mins following the hypoxic stimulus. In contrast, carotid body deactivation with hyperoxia (100% O 2 for 1 min) transiently reduced MSNA in eight of nine trials (mean decrease 12.6 ± 9.5%, p = 0.005). Our results suggest that input from the carotid chemoreceptors is obligatory for the sustained elevation in MSNA initiated by chemoreflex stimulation. We attribute the decrease in MSNA to a transient hyperoxia‐induced attenuation in carotid chemoreceptor sensitivity. Research support: NSERC, MSFHR
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Querido et al. (2009) studied this question.
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