title: Influence of atipamezole on effects of midsacral subarachnoidally administered detomidine in mares.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  10 healthy mares.
  
  
  METHODS
  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
  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.
authors.affiliation: Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus 43210-1089, USA.
authors.forename: R T
authors.initials: RT
authors.lastname: Skarda
authors.forename: W W
authors.initials: WW
authors.lastname: Muir
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000700:Analgesics / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001831:Body Temperature / Q000187:drug effects; D018592:Cross-Over Studies; D004347:Drug Interactions; D004558:Electric Stimulation; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006736:Horses; D007093:Imidazoles / Q000008:administration & dosage / Q000494:pharmacology*; D010146:Pain; D011897:Random Allocation; D012119:Respiration / Q000187:drug effects; D012447:Sacrum; D012677:Sensation / Q000187:drug effects; D016037:Single-Blind Method; D013346:Subarachnoid Space
chemical_list: D000317:Adrenergic alpha-Antagonists; D000700:Analgesics; D007093:Imidazoles; C050701:atipamezole; C041255:detomidine