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J Appl Physiol (December 10, 2004). doi:10.1152/japplphysiol.00749.2004
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Submitted on July 16, 2004
Accepted on December 8, 2004

INCREASED PROPENSITY FOR APNEA VIA DOPAMINE-INDUCED CAROTID BODY INHIBITION IN SLEEPING DOGS

Bruno J Chenuel1*, Curtis A Smith2, Kathleen S Henderson2, and Jerome A Dempsey2

1 Laboratoire de Physiologie, Faculte de Medecine de Nancy, Nancy, France; John Rankin Laboratory of Pulmonary Medicine and Department of Population Health Sciences, University of Wisconsin, Madison, Madison, WI, USA
2 John Rankin Laboratory of Pulmonary Medicine and Department of Population Health Sciences, University of Wisconsin, Madison, Madison, WI, USA

* To whom correspondence should be addressed. E-mail: bruno.chenuel{at}medecine.uhp-nancy.fr.

We determined the effects of specific carotid body chemoreceptor inhibition on the propensity for apnea during sleep. We reduced the responsiveness of the carotid body chemoreceptors using i.v. dopamine infusions during non-REM sleep in 6 dogs. Then, we quantified the difference in PETCO2 between eupnea and the apneic threshold, the "CO2 reserve" by gradually reducing PETCO2 transiently with pressure support ventilation at progressively increased VT until apnea occurred. Dopamine infusions decreased steady-state eupneic ventilation by 15% ± 6 % causing a mean CO2 retention of 3.9 ± 1.9 mmHg and a brief period of ventilatory instability. The apneic threshold PETCO2 rose +5.1 ± 1.9 mmHg; thus, the CO2 reserve was narrowed from -3.9 ± 0.62 mmHg in control to -2.7 ± 0.78 mmHg with dopamine. This decrease in the CO2 reserve with dopamine resulted solely from the 20.5 ± 11.3 % increase in plant gain; the slope of the ventilatory response to CO2 below eupnea was unchanged from normal. We conclude that specific carotid chemoreceptor inhibition with dopamine increases the propensity for apnea during sleep by narrowing the CO2 reserve below eupnea. This narrowing is due solely to an increase in plant gain as the slope of the ventilatory response to CO2 below eupnea was unchanged from normal control. These findings have implications for the role of chemoreceptor inhibition/stimulation in the genesis of apnea and breathing periodicity during sleep.




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