Central dopamine modulates anapyrexia but not hyperventilation induced by hypoxia.

Abstract

Hypoxia causes hyperventilation and decreases body temperature (T(b)) and metabolism [O(2) consumption (VO(2))]. Because dopamine (DA) is released centrally in response to peripheral chemoreceptor stimulation, we tested the hypothesis that central DA mediates the ventilatory, thermal, and metabolic responses to hypoxia. Thus we predicted that injection of haloperidol (a DA D(2)-receptor antagonist) into the third ventricle would augment hyperventilation and attenuate the drop in T(b) and VO(2) in conscious rats. We measured ventilation, T(b), and VO(2) before and after intracerebroventricular injection of haloperidol or vehicle (5% DMSO in saline), followed by a 30-min period of hypoxia exposure. Haloperidol did not change T(b) or VO(2) during normoxia; however, breathing frequency was decreased. During hypoxia, haloperidol significantly attenuated the falls in T(b) and VO(2), although hyperventilation persisted. The present study shows that central DA participates in the thermal and metabolic responses to hypoxia without affecting hyperventilation, showing that DA is not a common mediator of this interaction.