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Dexmedetomidine Hydrochloride Research Paper

955 Words4 Pages

DEXMEDETOMIDINE:

Dexmedetomidine hydrochloride is the dextrorotatory S-enantiomer of medetomidine and is chemically described as (S)-4-[1-(2,3-dimethylphenyl)ethyl]-3H-imidazole. It has a molecular weight of 236.7 and the empirical formula is C13H17CIN2 • HCl and the structural formula is:

Dexmedetomidine hydrochloride is a white powder that is freely soluble in water.

Mechanism Of Action
Dexmedetomidine, displays specific and selective α2-adrenoceptor agonism. It causes activation of the receptors in the brain and spinal cord inhibits neuronal firing, causing hypotension, bradycardia, sedation, and analgesia. The responses to activation of the receptors in other areas include decreased salivation, decreased secretion, and decreased bowel …show more content…

The majority of patients receiving dexmedetomidine as a primary therapy experienced clinically effective sedation yet were still easily arousable, a unique feature not observed with other clinically available sedatives.
Dexmedetomidine does not appear to have any direct effects on the heart . A biphasic cardiovascular response has been described after the application of dexmedetomidine. The administration of a bolus of 1 μg/kg dexmedetomidine initially results in a transient increase of the blood pressure and a reflex decrease in heart rate, especially in younger, healthy patients . The initial reaction can be explained by the peripheral α2B-adrenoceptor stimulation of vascular smooth muscle and can be attenuated by a slow infusion over 10 or more minutes. Even at slower infusion rates, however, the increase in mean arterial pressure over the first 10 minutes was shown to be in the range of 7%, with a decrease in heart rate between 16% and 18% . The initial response lasts for 5 to 10 minutes and is followed by a decrease in blood pressure of approximately 10% to 20% below baseline and a stabilization of the heart rate, also below baseline values; both of these effects are caused by the inhibition of the central sympathetic outflow overriding the direct stimulating effects . Another possible explanation for the subsequent heart rate decrease is the stimulation of the presynaptic α2-adrenoceptor, leading to a decreased norepinephrine

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