| Indication | For sedation of initially intubated and mechanically ventilated patients during treatment in an intensive care setting, also used in pain relief; anxiety reduction and analgesia |
| Pharmacodynamics | Dexmedetomidine activates 2-adrenoceptors, and causes the decrease of sympathetic tone, with attenuation of the neuroendocrine and hemodynamic responses to anesthesia and surgery; it reduces anesthetic and opioid requirements; and causes sedation and analgesia. |
| Mechanism of action | Dexmedetomidine is a specific and selective alpha-2 adrenoceptor agonist. By binding to the presynaptic alpha-2 adrenoceptors, it inhibits the release if norepinephrine, therefore, terminate the propagation of pain signals. Activation of the postsynaptic alpha-2 adrenoceptors inhibits the sympathetic activity decreases blood pressure and heart rate. |
| Absorption | Not Available |
| Volume of distribution | |
| Protein binding | 94% |
| Metabolism | Hepatic |
| Route of elimination | A mass balance study demonstrated that after nine days an average of 95% of the radioactivity, following intravenous administration of radiolabeled dexmedetomidine, was recovered in the urine and 4% in the feces. Fractionation of the radioactivity excreted in urine demonstrated that products of N-glucuronidation accounted for approximately 34% of the cumulative urinary excretion. The majority of metabolites are excreted in the urine. |
| Half life | 2 hours |
| Clearance | - 39 L/h [Healthy volunteers receiving IV infusion (0.2-0.7 mcg/kg/hr)]
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| Toxicity | Not Available |
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