Almitrine and the peripheral ventilatory response to CO2 in hyperoxia and hypoxia

Abstract

The effects of almitrine bismesylate (initial intravenous dose 0.6 mg·kg−1 followed by continuous infusion of 0.4 mg·kg−1·h−1) on the ventilatory response to CO2 during hyperoxia and hypoxia were determined in 6 anaesthestized cats with the use of the dynamics end-tidal CO2 forcing technique. It was found that almitrine almost doubled the peripheral ventilatory sensitivity to CO2 during hyperoxia (mean PetO2 45.6 kPa) and also during mild hypoxia (mean PetO2 8.7 kPa). The apnoeic threshold (B) was in both cases shifted to substantially lower values than those of the control measurements. No significant effects of almitrine were found on the central ventilatory sensitivity to CO2 either during hyperoxia or during hypoxia. It is argued that the decrease of the apnoeic threshold may be due to an inhibitory effect of almitrine on the carotid body dopaminergic activity, and that the increase of the sensitivity to CO2 stems from a “hypoxia mimetic” mechanism.