Serum doxapram and respiratory neuromuscular drive in normal man.

To investigate the means by which doxapram affects the control of ventilation, ventilatory function and P0.1 have been related to serum doxapram concentration during a 45-min infusion of doxapram hydrochloride in 7 healthy, conscious subjects under normoxic conditions. Serum doxapram concentrations increased during the infusion: 1.88, 2.48, 3.42, and 3.97 micrograms/ml after 5, 10, 30 and 45 min, respectively. The majority of significant changes in the measurements from the baseline were observed at 30 and 45 min: VE, VT, P0.1, P0.1/end-tidal CO2 tension, VT/Ti and blood pressure were increased, and end-tidal CO2 tension was decreased. No significant changes in Pdimax, Ti/Ttot, VE/P0.1, and P0.1/(VT/Ti) were observed. A correlation was observed between the % increases in P0.1 and VE and doxapram concentration, and between VE and P0.1. The doxapram-induced increase in VE appears to be caused by increased neural drive. It is related to the serum drug concentration in the conscious subject.