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Dexmedetomidine, sold under the brand name Precedex among others, is a medication used for sedation. [4] Veterinarians use dexmedetomidine for similar purposes in treating cats, dogs, and horses. [ 10 ] [ 11 ] It is also used in humans to treat acute agitation associated with schizophrenia or bipolar disorder . [ 5 ]
Medications such as clonidine and dexmedetomidine target pre-synaptic auto receptors, therefore leading to an overall decrease in norepinephrine which clinically can cause effects such as sedation, analgesia, lowering of blood pressure and bradycardia. There is also low quality evidence that they can reduce shivering post operatively.
Clonidine may improve symptoms of attention deficit hyperactivity disorder in some people but causes many adverse effects and the beneficial effect is modest. [22] In Australia, clonidine is an accepted but not approved use for ADHD by the TGA. [23] Clonidine, along with methylphenidate, has been studied for treatment of ADHD.
Clonidine is now thought to decrease blood pressure via this central mechanism. Other nonselective agonists include dexmedetomidine, lofexidine (another antihypertensive), TDIQ (partial agonist), tizanidine (in spasms, cramping) and xylazine. Xylazine has veterinary use.
They are mainly used in research, having found limited clinical application in human medicine. They are extensively used in veterinary medicine to reverse the effects of alpha-2 agonist drugs used as sedatives, like xylazine, medetomidine and dexmedetomidine. Alpha-2 blockers increase noradrenaline release.
Medetomidine is a racemic mixture of two optical or stereoisomers, levomedetomidine and dexmedetomidine. [4] The latter causes the alpha 2- adrenergic agonist effects. [5] It is often used as the hydrochloride salt, medetomidine hydrochloride, a crystalline white solid that can be administered as an intravenous drug solution with sterile water.
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Detomidine is a sedative with analgesic properties. [3] α 2-adrenergic receptor agonists produce dose-dependent sedative and analgesic effects, mediated by activation of α 2 catecholamine receptors, thus inducing a negative feedback response, reducing production of excitatory neurotransmitters.
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