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Physiological role of alpha 2-adrenoceptors in the regulation of vigilance and pain: effect of medetomidine.

Abstract
The sedative action of alpha 2-adrenergic agonists is generally ascribed to inhibition of the locus coeruleus (LC) and its ascending activating projection to the forebrain, although postsynaptic effects in the neocortex may also play a part. The sedative effect of the drugs varies considerably between different species. Systemic application of alpha 2-adrenergic agents have analgesic effects in addition to their sedative actions. Descending noradrenergic projections from the LC area modulate pain transmission at the spinal level. The purpose of this trial was to investigate the sedative properties of medetomidine in the cat. Medetomidine was injected intramuscularly at dose rates of 0.02, 0.06 and 0.18 mg/kg. Xylazine 3.0 mg/kg and saline were used for comparison. Medetomidine increased drowsy waking at the expense of both arousal and sleep. Nociceptive reflexes were suppressed in the case of the smallest dose of medetomidine, and abolished by the others. The 0.18 mg/kg dose of medetomidine had approximately equal effect on vigilance as 3.0 mg/kg of xylazine. The duration of the effect of medetomidine was dose-dependent. The alpha-receptor blocker phentolamine i.m. reversed the heavy sedation produced by medetomidine. Medetomidine also produced significant bradycardia, but the duration of this effect was not dose-dependent.
AuthorsD Stenberg
JournalActa veterinaria Scandinavica. Supplementum (Acta Vet Scand Suppl) Vol. 85 Pg. 21-8 ( 1989) ISSN: 0065-1699 [Print] Denmark
PMID2571274 (Publication Type: Journal Article, Review)
Chemical References
  • Adrenergic alpha-Agonists
  • Hypnotics and Sedatives
  • Imidazoles
  • Receptors, Adrenergic, alpha
  • Medetomidine
Topics
  • Adrenergic alpha-Agonists (pharmacology)
  • Anesthesia
  • Animals
  • Arousal (drug effects, physiology)
  • Cats
  • Humans
  • Hypnotics and Sedatives (pharmacology)
  • Imidazoles (pharmacology)
  • Medetomidine
  • Pain (drug therapy, metabolism)
  • Receptors, Adrenergic, alpha (physiology)

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