Refinement of the dose of doxapram to counteract the sedative effects of acepromazine in dogs.

OBJECTIVES: To evaluate the effectiveness of two doses of doxapram in reversing acepromazine sedation in dogs. METHODS: Using a crossover design, 10 adult mixed-breed dogs received 0·05 mg/kg acepromazine, intramuscularly (im) followed 30 minutes later by one of the three randomly determined treatments: 0·0625 mL/kg saline, intravenously (iv), 1·25 mg/kg doxapram, iv or 2·5 mg/kg doxapram, iv. Sedation scores were obtained by a single, blinded observer at 0, 15 and 30 minutes after acepromazine administration and at 5, 15 and 30 minutes after the treatment administration. RESULTS: The mean baseline sedation score of all the treatments was not different among treatments. All the dogs had a significant increase in sedation score at 30 minutes after acepromazine administration. Both the low and high doses of doxapram showed a significant decrease in sedation score compared to saline, but there was no significant difference between the two doses. Five dogs in the high dose group panted after treatment injection, and this was significantly more than in the low dose group. CLINICAL SIGNIFICANCE: Doxapram is effective in reducing the sedative effects of acepromazine over a short period of time. A dose of 1·25 mg/kg effectively decreases acepromazine sedation without causing panting.

Acepromazine-xylazine combination in dogs: antagonism with 4-aminopyridine and yohimbine.

Groups of fasted atropinized crossbred dogs of both sexes were injected IM with a standard dosage of a xylazine-acepromazine combination (2.2 mg/kg and 0.5 mg/kg, respectively). Righting reflex was uniformly lost and considered to be the point of maximum sedation. After maximal sedation, dogs were injected IV with 4-amino-pyridine (4-AP, 0.5 mg/kg), yohimbine (0.25 mg/kg), or a combination of 4-AP and yohimbine. Controls were given (IV) 1 ml of saline solution. The 4-AP, yohimbine, and 4-AP + yohimbine significantly reduced walk times (time to arousal and ability to walk on a leash) from a control value of 43.1 minutes to 7.6, 4.4, and 1.9 minutes, respectively (P less than 0.05). Relapse to unconsciousness did not occur with any antagonist regimen and recovery was uneventful. In 3 dogs sedated with the xylazine-acepromazine combination supplemented with halothane having surgically placed cannulas and electrodes for measurement of electroencephalo-, electrocardio-, and electromyographic (EEG, ECG, and EMG) responses, arterial blood pressure, and respiratory rates and depth, IV injection of 4-AP + yohimbine caused transient femoral arterial hypotension with tachycardia, increases in respiratory rate, depth, and minute volume, increased EMG and EEG activities preceding and accompanying gross movements, slight speeding of ECG, and behavioral arousal within 3 minutes. Increased heart rate also was observed in intact dogs given yohimbine. Increased rate and depth of respiration also was seen in all intact dogs given antagonists. Curiously, the xylazine-acepromazine combination did not induce arterial hypotension as expected from the product literature. To what extent pretreatment with atropine sulfate may have counteracted this effect is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of etorphine-acepromazine and diprenorphine in reversible neuroleptanalgesia of rats.

The death rate due to neuroleptanalgesia (0.35%) was significantly lower than for barbiturate anaesthesia (1.59%). Complications were few even when animals received multiple, repeated, anaesthesia, and depth of anaesthesia could be adjusted easily. Further, it could be reversed within minutes by the specific antagonist diprenorphine.