Seventy-two healthy dogs required sedation and analgesia for a variety
of procedures causing discomfort or pain, They were treated either wi
th the alpha(2)-agonist medetomidine at 40 mu g/kg (15 intravenously a
nd 17 intramuscularly), or 80 mu g/kg (15 intravenously and 15 intramu
scularly) or with xylazine plus 1-methadone (1.0 mg) (10 intravenously
), The levels of sedation, analgesia and safety were compared clinical
ly and by measurements of the effects on the electrocardiogram (ECG) a
nd blood gases, body temperature, haematology and clinical chemistry,
Sedation was achieved reliably with both medetomidine and xylazine plu
s I-methadone but its onset, depth and duration were influenced by the
dose and route of administration, In the medetomidine-treated dogs, i
ntravenous administration resulted in more rapid sedation and the effe
cts of the higher dose were deeper and longer lasting, The small dogs
receiving 40 mu g/kg may have been underdosed. The initial analgesic e
ffects in response to a pin prick to the body surface were sufficient
and similar for both drugs, except for the intramuscular dose of 40 mu
g/kg medetomidine. Analgesia for the clinical procedures was less rel
iable with medetomidine and was not always adequate even at the high d
ose, but xylazine plus 1-methadone assured analgesia in almost every c
ase, Medetomidine resulted in marked bradycardia, lasting as long as t
he sedation and the ECG revealed a sinus arrhythmia with sinoatrial an
d atrioventricular blocks grade I and II as a sign of interference wit
h transduction, The bradycardia with xylazine plus 1-methadone was les
s pronounced. A decrease in respiratory rate accompanying sedation had
no influence on blood gases and blood acidity in the dogs treated wit
h medetomidine but caused a respiratory acidosis with xylazine plus I-
methadone, Body temperature decreased with all treatments for the dura
tion of the period of sedation, Blood glucose concentration increased
to a similar extent in all treatment groups, but all other haematologi
cal and clinicochemical variables remained unchanged, Treatment with t
he specific alpha(2) antagonist, atipamezole, reversed the sedation an
d cardiovascular and pulmonary effects due to medetomidine within minu
tes.