| 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)]
|
| Toxicity |
Not Available |
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