Abstract

Intravenous administration of dopamine suppresses ventilation in man through an effect on the chemoreceptor reflex. The primary goal of this study was to determine if a dopaminergic blocking agent, haloperidol, alters the ventilatory response to dopamine in man. Dopamine was infused intravenously in 10 normal men during hypoxia, before and after 2.5 mg of haloperidol intramuscularly, to block dopaminergic receptors. Before haloperidol, dopamine (5 micrograms/kg/min) decreased minute ventilation 1.7 +/- 0.5 liters/min (P less than .05) and increased arterial pCO2 3.5 +/- 0.6 mm Hg (P less than .05). After haloperidol, dopamine did not alter ventilation. The findings suggest that inhibition of the chemoreceptor reflex by dopamine in man is mediated by dopaminergic receptors. A secondary goal of this study was to test the hypothesis that, if dopamine is an inhibitory transmitter in chemoreceptors, blockade of dopaminergic receptors would increase ventilation. Haloperidol did not alter minute ventilation or arterial pCO2 during normoxia or hypoxia. The observation that haloperidol blocks the response to exogenous dopamine, but does not alter ventilation during normoxia or hypoxia, suggests that either endogenous dopamine does not play an important role in determining steady-state chemoreceptor discharge or endogenously released dopamine may have access to receptors that are relatively inaccessibly to exogenous blockers.