Xylazine was administered intravenously at a dosage level of 0.2 mg/kg to 7 calves and changes in EEG were examined. The EEG was recorded using needle electrodes by monopolar recording in the bilateral frontal and occipital areas. In the EEG tracing before xylazine administration, low-amplitude (about 10μV) β waves were predominant and 10 to 20 μV a waves and 20 to 30 μV θ waves were also observed. Furthermore, part of β waves were superimposed on θ waves. Slow waves with a frequency of 3 Hz or less (δ waves) appeared 1 to 2 min after xylazine administration and persisted for about 20 min. The amplitude of δ waves often exceeded beyond 100μV, and those in the occipital area were higher than those in the frontal area. The incidence and amplitude ofδ waves were decreased and the incidences of a and β waves were increased 30 min or more after xylazine administration. The EEG findings obtained 90 min after xylazine administration were almost the same as before the administration. When photic stimulation was given at 10 and 60 min after xylazine administration, photic driving which was predominant in the occipital area was observed in all animals.

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Incidence of ventricular premature contractions (VPC) induced by thiopental sodium alone or thiopental sodium with premedicant administrations were evaluated utilizing 78 beagle dogs. Twenty four out of 78 beagles (30.8%) produced VPC when 25 mg/kg of thiopental sodium were slowly (60 sec) administered intravenously. Twenty four beagles that produced VPC were re-evaluated by an administration of thiopental sodium, which resulted in the increased incidence of VPC in 19 dogs (79.2%) . Fifteen beagles among 19 were administered thiopental sodium until eyelid closure reflex disappeared with combinations of droperidol, propionylpromazine and diazepam under the influence of atropine sulphate. A slight decrease in the incidence of VPC was observed with these premedicants administrations. It is probably due to the decreased doses of thiopental sodium administration.

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Epidural anesthesia is not prevalent in the dog but general anesthesia has been therefore attained through inhalation or various injection methods modified by each veterinarian's ingenuity. In the present experiment, we conducted epidural anesthesia in the dog to maintain and prolong the analgesia after the initial induction.
After the anesthesia with diazepam and ketamine hydrochloride, an injection needle was inserted into the epidural space via the lumbar vertebra to introduce a catheter. When 0.4 ml/kg of 2% lidocaine hydrochloride was injected through the catheter, the area from T11 to S2 segments was innervated and analgesic for 30 to 60 minutes. This condition was maintained for 110 to 150 minutes when 0.2 ml/kg of the anesthetic was added twice. The degree or extent of analgesia varied among the animals according to the location of the catheter end or the dog's posture: in some cases analgesia extended to T₄ or C₈ segment, while in others the lower side of the body remained analgesia for longer time. The cardiopulmonary functions were not affected in all cases.

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