Almitrine increases breathing by stimulating peripheral chemoreceptors. Previous studies suggest clinical usefulness in the adult with
chronic obstructive pulmonary disease, but little data are available to decide whether
almitrine would be helpful in diseases involving pharyngeal
airway obstruction, such as
apnea of prematurity or
obstructive sleep apnea. We investigated the effect of intravenous
almitrine on hypoglossal (HG), an upper airway nerve, and phrenic (PHR) neural activity in eight
alpha-chloralose-
urethan anesthetized, paralyzed, vagotomized, and artificially ventilated cats. Recordings were made of raw and integrated HG and PHR electroneurograms (ENGs), alveolar PCO2, arterial PO2, arterial blood pressure, and rectal temperature. A dose-response study of cumulative
almitrine doses ranging from 0.1 to 4.0 mg/kg was performed in three cats. The interactive effects of
almitrine and hypoxic stimulation were investigated in four cats. The interactive effects of
almitrine and hypercapnic stimulation were investigated in five cats. The interactive effects of
almitrine and ventilatory timing were investigated in six cats. We found that 1)
almitrine doses as low as 0.1 mg/kg iv increased both HG and PHR ENG activity, with a maximum effect at approximately 1.0 mg/kg; 2)
almitrine markedly increased HG and PHR ENG activity at all arterial PO2 values from 35-175 Torr; 3)
almitrine increased HG and PHR ENG activity at all arterial PCO2 values from 30-70 Torr; and 4)
almitrine increased the ratio of tidal volume to inspiratory time and decreased the inspiratory muscle duty cycle at normoxia and eucapnia.