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Related Experiment Videos

Peripheral chemoreflex function in hyperoxia following ventilatory acclimatization to altitude.

M E Pedersen1, P Robach, J P Richalet

  • 1University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, United Kingdom.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 25, 2000
PubMed
Summary

Persistent hyperventilation after high altitude acclimatization is not driven by carotid body activity. Dopamine, a carotid body inhibitor, did not alter ventilation in hyperoxia, refuting this hypothesis.

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Area of Science:

  • Physiology
  • Altitude Medicine
  • Respiratory Control

Background:

  • Ventilatory acclimatization to high altitude (VAH) results in persistent hyperventilation even when the hypoxic stimulus is removed.
  • This sustained hyperventilation may be partly due to altered acid-base status or persistent carotid body (CB) activity.
  • The hypothesis tested is that a component of CB activity develops during VAH that is resistant to suppression by hyperoxia.

Purpose of the Study:

  • To investigate the role of carotid body (CB) activity in persistent hyperventilation after ventilatory acclimatization to high altitude (VAH).
  • To determine if inhibiting the CB with dopamine affects ventilation during hyperoxia following VAH.

Main Methods:

  • Eight volunteers underwent simulated high-altitude ascent in a hypobaric chamber.

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  • Acute hyperoxia exposure was administered at various acclimatization stages.
  • Carotid body inhibition was achieved using dopamine infusion (3 microg.kg(-1).min(-1)) during the latter 10 minutes of hyperoxia.
  • Main Results:

    • Ventilation significantly increased (P < 0.001) and end-tidal PCO(2) significantly decreased (P < 0.001) with VAH.
    • Dopamine infusion during hyperoxia did not progressively affect ventilation or end-tidal PCO(2) in subjects with VAH.
    • These findings indicate that the CB does not generate the persistent hyperventilation observed in hyperoxia post-VAH.

    Conclusions:

    • The carotid body (CB) does not appear to play a significant role in generating persistent hyperventilation after ventilatory acclimatization to high altitude (VAH) when exposed to hyperoxia.
    • The persistent hyperventilation observed in hyperoxia after VAH is likely mediated by factors other than sustained carotid body activity.
    • Further research is needed to elucidate the precise mechanisms underlying persistent hyperventilation post-VAH.