Effects of three methadone doses combined with acepromazine on sedation and some cardiopulmonary variables in dogs.

OBJECTIVE: To evaluate the sedative and cardiopulmonary effects of three methadone doses, combined with acepromazine, in dogs. STUDY DESIGN: Prospective, randomized, complete block study. ANIMALS: Six healthy, adult, cross-bred dogs weighing 17.2±4.4 kg (mean±standard deviation). METHODS: Each dog was administered four treatments: acepromazine (0.05 mg kg-1) alone or acepromazine (same dose) in combination with methadone (0.25, 0.50 or 0.75 mg kg-1). All drugs were administered intramuscularly. Sedation was scored by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 0-10). Heart rate, invasive blood pressure, arterial blood gases and rectal temperature were measured at 15 to 30 minute intervals for 120 minutes. RESULTS: According to NDS scores, mild to moderate sedation (NDS=1-2) was observed in most dogs in the acepromazine treatment, with only one out of six dogs scored as exhibiting intense sedation (NDS=3). All treatments with methadone resulted in significantly higher SNS scores compared with acepromazine alone. In these treatments, most dogs exhibited intense sedation (NDS=3). Increasing the dose of methadone from 0.25 to 0.50 or 0.75 mg kg-1 prolonged sedation in a dose-related manner, but did not influence the degree of sedation. The main adverse effects following administration of acepromazine-methadone treatments were decreased blood pressure, mild respiratory acidosis and decreased rectal temperature. These effects were well tolerated and resolved without treatment. CONCLUSIONS AND CLINICAL RELEVANCE: In this study in six dogs, acepromazine-methadone administration resulted in intense sedation in most dogs. The results are interpreted to indicate that a low dose of methadone (0.25 mg kg-1) administered in combination with acepromazine (0.05 mg kg-1) will induce short-term sedation in dogs, whereas higher doses of methadone should be administered when prolonged sedation is desired.

Effects of a prolonged infusion of fentanyl, with or without atropine, on the minimum alveolar concentration of isoflurane in dogs.

OBJECTIVES: To evaluate the effect of a prolonged constant rate infusion (CRI) of fentanyl on the minimum alveolar concentration (MAC) of isoflurane (ISOMAC ) and to establish whether concurrent atropine administration influences ISOMAC in dogs. STUDY DESIGN: Prospective, crossover study. ANIMALS: Six healthy dogs weighing 13.0 ± 4.1 kg. METHODS: Dogs were anesthetized with isoflurane under conditions of normocapnia and normothermia. Arterial blood pressure was monitored invasively. Each dog was administered two treatments, on different occasions, in a crossover design. The dogs were administered intravenously (IV) an atropine bolus 0.02 mg kg(-1) and CRI at 0.04 mg kg(-1) hour(-1) (fentanyl-atropine treatment) or no atropine (fentanyl treatment). For each dog, baseline ISOMAC was measured in duplicate using a tail clamp technique. Subsequently, all dogs were administered a fentanyl bolus (5 µg kg(-1)) and CRI (9 µg kg(-1) hour(-1)) IV, and ISOMAC was re-determined at 120 and 300 minutes after initiation of the fentanyl CRI. RESULTS: Baseline ISOMAC values in the fentanyl and fentanyl-atropine treatments were 1.38 ± 0.16% and 1.39 ± 0.14%, respectively. Fentanyl significantly decreased the ISOMAC by 50 ± 9% and 47 ± 13% after 120 minutes and by 51 ± 14% and 50 ± 9% after 300 minutes (p < 0.001) in the fentanyl and fentanyl-atropine treatments, respectively. Compared with baseline, heart rate decreased significantly in the fentanyl treatment by 35% and 43% at 120 and 300 minutes, respectively. In the fentanyl-atropine treatment, heart rate did not change significantly over time. In both treatments, systolic arterial pressure increased from baseline after fentanyl. CONCLUSIONS AND CLINICAL RELEVANCE: In this study, fentanyl reduced the ISOMAC by approximately 50%. The ISOMAC remained stable throughout the 300 minute CRI of fentanyl, suggesting no cumulative effect of the opioid. Atropine did not influence ISOMAC in dogs.

Randomized clinical trial of the effects of a combination of acepromazine with morphine and midazolam on sedation, cardiovascular variables and the propofol dose requirements for induction of anesthesia in dogs.

The present study evaluated the effects of acepromazine combined with midazolam and morphine on sedation and cardiovascular variables as well as the propofol dose required for induction of anesthesia in dogs compared with acepromazine-morphine or midazolam-morphine. Dogs were randomly assigned to receive an intramuscular administration of (1) acepromazine (0.05 mg/kg) with 0.5mg/kg of morphine (group AM, n=10), (2) midazolam (0.5mg/kg) with 0.5mg/kg of morphine (group MM, n=9), or (3) acepromazine with midazolam and morphine at the same doses (group AMM, n=10). After 30 min, sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 0-10). Dogs were then administered IV propofol to allow endotracheal intubation. NDS and SNS scores were significantly higher in the AMM than in the MM group (P<0.05). There was a trend towards more dogs presenting with intense sedation (NDS=3) in AMM (6/10 dogs) compared with AM (1/10 dogs) and MM (1/9 dogs) (P=0.057). The propofol dose required for induction of anesthesia was significantly lower in AMM (4.0mg/kg) compared with MM (6.0mg/kg, P<0.01) but not AM (4.6 mg/kg). Heart rate decreased in AM after treatment and after intubation. Blood pressure decreased in groups AM and AMM following treatment and in all groups after intubation. The combination AMM resulted in intense sedation more frequently than AM and MM, and provided the greatest sparing effect in the propofol dose. Administration of AM and AMM but not MM decreased blood pressure although hypotension was not recorded in healthy dogs.