500 Torr; ref, 23) suggesting a
powerful inhibitory effect of hypocapnia at the carotid chemosensor
over a range of PCO2 encountered commonly in physiological
hyperpneas. The primary aim of this study was to assess the
ventilatory effect of CB hypocapnia on the ventilatory response to
concomitant CB hypoxia. The secondary aim was to assess the relative
gains of the CB and central chemoreceptors to hypocapnia . In 8
awake, female dogs the vascularly-isolated CB was perfused with
hypoxic blood (mild, PCBO2 50 Torr or severe, PCBO2 36 Torr) in a
background of normocapnia or hypocapnia (10 Torr < eupneic PaCO2) in
the perfusate. The systemic (and brain) circulation was normoxic
throughout and PaCO2 was not controlled (poikilocapnia). CB
Hypocapnia: The peak ventilation (range 19-27 sec) in response to
hypoxic CB perfusion increased 48% (mild) and 77% (severe) due to
increased VT. When CB hypocapnia was present these increases in were
reduced to 21% and 27% respectively. Systemic Hypocapnia: With the
isolated CB maintained normocapnic and hypoxic for >70 seconds
the steady-state poikilocapnic ventilatory response (i.e. to systemic
hypocapnia alone) decreased 15% (mild CB hypoxia) and 27% (severe CB
hypoxia) from the peak response. We conclude that carotid body
hypocapnia can be a major source of inhibitory feedback to
respiratory motor output during the hyperventilatory response to
hypoxic carotid body stimulation.
Received 6 June 1996; accepted in final form 28 October 1996.
APS Manuscript Number A524-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996