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Influence of atipamezole on effects of midsacral subarachnoidally administered detomidine in mares.

AbstractOBJECTIVE:
To examine effects of atipamezole on detomidine midsacral subarachnoidally-induced analgesia, cardiovascular and respiratory activity, head ptosis, and position of pelvic limbs in healthy mares.
ANIMALS:
10 healthy mares.
PROCEDURE:
Using a randomized, blinded, crossover study design, mares received detomidine (0.03 mg/kg of body weight, diluted in 3 ml of CSF) midsacral subarachnoidally, followed by atipamezole (0.1 mg/kg [test]) or sterile saline (0.9% NaCl) solution (control), i.v. 61 minutes later and saline solution (3 ml, midsacral subarachnoidally) on a separate occasion, at least 2 weeks later. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle-prick stimulation extending from the coccygeal to T15 dermatomes. Arterial acid-base (pH, standard bicarbonate, and base excess values), gas tensions (PO2, PCO2), PCV, total solids concentration, heart and respiratory rates, rectal temperature, and arterial blood pressure were determined, and mares were observed for sweating and urination. Mean scores of perineal analgesia, head ptosis, position of pelvic limbs, and cardiovascular and respiratory data were compared for the 3-hour test period.
RESULTS:
Subarachnoidally administered detomidine induced perineal analgesia (mean +/- SD onset, 9.0 +/- 4.6 minutes; duration, 130 +/- 26 minutes), marked head ptosis, moderate changes in pelvic limb position, cardiovascular and respiratory depression, sweating in analgesic zones, and diuresis. Intravenously administered atipamezole significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, pelvic limb position, sweating and diuresis; partially antagonized detomidine-induced bradycardia; and did not effect detomidine-induced bradypnea.
CONCLUSIONS AND CLINICAL RELEVANCE:
Most effects of midsacral subarachnoidally administered detomidine, except bradycardia and bradypnea, were reversed by atipamezole (0.1 mg/kg, i.v.), indicating that most of the actions of detomidine were mediated via activation of alpha2-adrenergic receptors.
AuthorsR T Skarda, W W Muir 3rd
JournalAmerican journal of veterinary research (Am J Vet Res) Vol. 59 Issue 4 Pg. 468-77 (Apr 1998) ISSN: 0002-9645 [Print] United States
PMID9563633 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Adrenergic alpha-Antagonists
  • Analgesics
  • Imidazoles
  • atipamezole
  • detomidine
Topics
  • Acid-Base Equilibrium (drug effects)
  • Adrenergic alpha-Antagonists (pharmacology)
  • Analgesics (administration & dosage, pharmacology)
  • Animals
  • Blood Pressure (drug effects)
  • Body Temperature (drug effects)
  • Cross-Over Studies
  • Drug Interactions
  • Electric Stimulation
  • Female
  • Heart Rate (drug effects)
  • Horses
  • Imidazoles (administration & dosage, pharmacology)
  • Pain
  • Random Allocation
  • Respiration (drug effects)
  • Sacrum
  • Sensation (drug effects)
  • Single-Blind Method
  • Subarachnoid Space

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