Source: FDA, National Drug Code (US) Revision Year: 2021
Doxapram hydrochloride produces respiratory stimulation mediated through the peripheral carotid chemoreceptors. As the dosage level is increased, the central respiratory centers in the medulla are stimulated with progressive stimulation of other parts of the brain and spinal cord.
The onset of respiratory stimulation following the recommended single intravenous injection of doxapram hydrochloride usually occurs in 20 to 40 seconds with peak effect at 1 to 2 minutes. The duration of effect may vary from 5 to 12 minutes.
The respiratory stimulant action is manifested by an increase in tidal volume associated with a slight increase in respiratory rate.
A pressor response may result following doxapram administration. Provided there is no impairment of cardiac function, the pressor effect is more marked in hypovolemic than in normovolemic states. The pressor response is due to the improved cardiac output rather than peripheral vasoconstriction. Following doxapram administration, an increased release of catecholamines has been noted.
Although opiate-induced respiratory depression is antagonized by doxapram, the analgesic effect is not affected.
Doxapram is metabolized via ring hydroxylation to ketodoxapram, an active metabolite readily detected in the plasma.
No carcinogenic or mutagenic studies have been performed using doxapram. Doxapram did not adversely affect the breeding performance of rats.
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