The Ventilatory Effects of Doxapram in Normal Man

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Abstract
To determine the mode of action of doxapram in man, ventilation, O2 uptake, CO2 production, hypoxic and hypercapnic ventilatory responses were measured in 6 healthy men before and during i.v. infusion to maintain a constant plasma level. Doxapram changed neither resting O2 uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. Doxapram increased the ventilatory response to isocapnic hypoxia from -0.8 .+-. 0.4 l min-1 (%SaO2 [arterial O2 saturation])-1 to -1.63 .+-. 0.9 l min-1 (%SaO2)-1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa [Pascal] without adding doxapram. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 .+-. 5.3 l min-1 kPa-1 to 20.4 .+-. 9.8 l min-1 kPa-1 during doxapram infusion. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanesthetized subjects.