Ventilatory effects of doxapram in conscious human subjects.
The ventilatory effects of a bolus intravenous dose of doxapram (0.37 to 0.47 mg/kg) were studied in ten healthy normal subjects. An immediate significant (p less than 0.001) increase in minute ventilation (VE) was due, in equal part, to significant increases in tidal volume (VT) and frequency (f). The inspiratory (TI) and expiratory time (TE) per breath decreased significantly. Mouth occlusion pressure increased significantly, in association with the increase in VT; there was no change in the ratio of VE to mouth occlusion pressure, indicating that respiratory mechanics did not alter. These results indicate that doxapram increases ventilation in conscious, normal man by an increase in inspiratory neuromuscular drive and a change in central breath timing. The ventilatory and mouth occlusion pressure responses to progressive isocapnic hypoxia and progressive hyperoxic hypercapnia were significantly altered by an intravenous infusion of doxapram (1 mg/min) only in the elevations (Y-intercepts) of the slopes of VE and mouth occlusion pressure; the regression coefficients did not change significantly. These results indicate that in conscious normal subjects, doxapram acts on both the peripheral and central respiratory receptors.
D000328:Adult; D002245:Carbon Dioxide / Q000032:analysis; D002628:Chemoreceptor Cells / Q000187:drug effects; D003243:Consciousness; D004315:Doxapram / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D007263:Infusions, Parenteral; D008297:Male; D010100:Oxygen / Q000032:analysis; D012119:Respiration / Q000187:drug effects*; D012129:Respiratory Function Tests; D013990:Tidal Volume
D002245:Carbon Dioxide; D004315:Doxapram; D010100:Oxygen