Seventy-two healthy dogs required sedation and analgesia for a variety of procedures causing discomfort or pain. They were treated either with the α2-agonist medetomidine at 40 μg/kg (15 intravenously and 17 intramuscularly), or 80 μg/kg (15 intravenously and 15 intramuscularly) or with xylazine plus 1- methadone (1.0 mg) (10 intravenously). The levels of sedation, analgesia and safety were compared clinically and by measurements of the effects on the electrocardiogram (ECG) and blood gases, body temperature, haematology and clinical chemistry. Sedation was achieved reliably with both medetomidine and xylazine plus I-methadone but its onset, depth and duration were influenced by the dose and route of administration. In the medetomidine-treated dogs, intravenous administration resulted in more rapid sedation and the effects of the higher dose were deeper and longer lasting. The small dogs receiving 40 μg/kg may have been underdosed. The initial analgesic effects in response to a pin prick to the body surface were sufficient and similar for both drugs, except for the intramuscular dose of 40 μg/kg medetomidine. Analgesia for the clinical procedures was less reliable with medetomidine and was not always adequate even at the high dose, but xylazine plus 1-methadone assured analgesia in almost every case. Medetomidine resulted in marked bradycardia, lasting as long as the sedation and the ECG revealed a sinus arrhythmia with sinoatrial and atrioventricular blocks grade I and II as a sign of interference with transduction. The bradycardia with xylazine plus 1-methadone was less pronounced. A decrease in respiratory rate accompanying sedation had no influence on blood gases and blood acidity in the dogs treated with medetomidine but caused a respiratory acidosis with xylazine plus 1-methadone. Body temperature decreased with all treatments for the duration of the period of sedation. Blood glucose concentration increased to a similar extent in all treatment groups, but all other haematological and clinicochemical variables remained unchanged. Treatment with the specific α2 antagonist, atipamezole, reversed the sedation and cardiovascular and pulmonary effects due to medetomidine within minutes.