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Background
Doxapram is a strong, dose-dependent respiratory stimulant in mammals. The oral LD50 in rats is 211mg/kg [1]. After Doxapram treatment, it has been noted a pressor response action through stimulation of the central nervous system (CNS). In addition, Doxapram has shown not only the central sensitization but also the prtipheral sensitization to hypercarbia in both animal and human studies. Furthermore, Doxapram has been reported to stimulate the carotid body in a dose-dependent fashion and have an additive but not synergistic effect on the carotid body response to hupercapnia. Apart from these, Doxapram has also shown the potent, direct and inhibitory effects on cloned TASK-1 and TASK-3 channels with the EC50 values of 410nM, 37nM and 9nM for TASK-1, TASK-3 and TASK-1/TASK-3, respectively. Doxapram has been revealed to augment neuromuscular transmission in a dose-related manner above a threshold concentration of 50μM [1].
[1] Yost CS. A new look at the respiratory stimulant doxapram. CNS Drug Rev. 2006 Fall-Winter;12(3-4):236-49.
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