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Increased propensity for apnea via dopamine-induced carotid body inhibition in sleeping dogs

¹Laboratoire de Physiologie, EA 3450, Faculté de Médecine de Nancy, Université Henri, Poincaré, France; and ²John Rankin Laboratory of Pulmonary Medicine and Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin

Submitted 16 July 2004 ; accepted in final form 8 December 2004

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 intravenous dopamine infusions during non-rapid eye movement sleep in six dogs. Then we quantified the difference in end-tidal PCO₂ (PET_CO2) between eupnea and the apneic threshold, the "CO₂ reserve," by gradually reducing PET_CO2 transiently with pressure support ventilation at progressively increased tidal volume 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 PET_CO2 rose 5.1 ± 1.9 Torr; thus the CO₂ reserve was narrowed from –3.9 ± 0.62 Torr in control to –2.7 ± 0.78 Torr 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.

sleep apnea; chemoreceptors; hypoventilation; apneic threshold; CO₂ reserve

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