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 Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of three acepromazine doses on the incidence of morphine-induced vomiting, sedation and some physiological variables in dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the incidence of vomiting was assessed. There was no significant difference between groups on the incidence of vomiting recorded in Phase 1, Phase 2 and the average of Phases 1 and 2. A significant decrease in PR was observed in most groups but no significant difference was detected between groups. Blood pressure decreased in all groups; during most of the evaluation period, SAP, MAP and DAP were significantly higher in the Control than in other treatments. Dogs in this study presented mild to intense sedation.[...]

Effects of Three Acepromazine Doses on the Incidence of Morphine-Induced Vomiting, Sedation and Some Physiological Variables in Dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the in

Effects of three acepromazine doses on the incidence of morphine-induced vomiting, sedation and some physiological variables in dogs

Background: Acepromazine was found to reduce the incidence of vomiting induced by opioids such as morphine, hydromorphone and oxymorphone in dogs. Despite the effectiveness of the phenothiazine in preventing opioid-induced vomiting in this species, a single dose of acepromazine (0.05 mg/kg) was tested and the influence of dose on the antiemetic effect of the drug is unknown. The primary objective of this study was to evaluate the effect of three acepromazine doses on the incidence of vomiting induced by morphine in dogs. A secondary aim was to assess the degree of sedation and effects on physiological variables following administration of the combinations tested.Materials, Methods & Results: All dogs received 0.5 mg/kg morphine (IM). Fifteen min before morphine, dogs in the Control, ACPLD, ACPMD and ACPHD groups were administered (IM) physiological saline or acepromazine at doses of 0.025, 0.05 and 0.1 mg/kg, respectively. In Phase 1, purpose-bred dogs (n = 8) underwent each of the four treatments in a randomized, crossover design; the incidence of vomiting, sedation, pulse rate (PR), systolic, mean and diastolic blood pressures (SAP, MAP and DAP) were investigated for 60 min. Sedation was assessed by a numeric descriptive scale (NDS, range 0-3) and a simple numerical scale (SNS, range 1-10). In Phase 2, client-owned dogs (n = 50) received a single treatment and only the incidence of vomiting was assessed. There was no significant difference between groups on the incidence of vomiting recorded in Phase 1, Phase 2 and the average of Phases 1 and 2. A significant decrease in PR was observed in most groups but no significant difference was detected between groups. Blood pressure decreased in all groups; during most of the evaluation period, SAP, MAP and DAP were significantly higher in the Control than in other treatments. Dogs in this study presented mild to intense sedation.[...](AU)

Efeitos antinociceptivos e sedativos da buprenorfina, da acepromazina ou da associação buprenorfina e acepromazina em gatos / Antinociceptive and sedative effects of buprenorphine, acepromazine, or combination of both, in conscious cats

O efeito antinociceptivo da buprenorfina tem sido relatado em cães e gatos. No presente estudo, avaliou-se o limiar nociceptivo mecânico em felinos tratados com buprenorfina, acepromazina ou ambas associadas e foram comparados os efeitos antinociceptivos e sedativos da associação em relação ao uso isolado desses fármacos determinados pelo mesmo observador, por meio de analgesiômetro e da escala analógica visual dinâmica interativa (DIVAS), respectivamente. Os oito animais empregados no estudo foram previamente familiarizados com os procedimentos utilizados. Após quatro mensurações basais, foram administrados, por via intramuscular, 0,02mg kg-1 de buprenorfina, 0,06mg kg-1 de acepromazina ou 0,01mg kg-1 de buprenorfina associada a 0,03mg kg-1 de acepromazina, em um estudo cego, com delineamento em quadrado latino e tratamento semanal. Os efeitos antinociceptivos e sedativos foram avaliados aos 15, 30, 45 minutos e uma, duas, três, quatro, seis, oito e 12 horas após a administração do tratamento. O limiar nociceptivo mecânico se elevou significativamente apenas no grupo tratado com a associação buprenorfina-acepromazina (entre 45 minutos e uma hora). Em relação à sedação, nos grupos tratados com acepromazina e com a associação, os valores da DIVAS foram significativamente maiores, respectivamente, de 15 minutos até quatro horas e de 15 minutos até três horas pós-tratamento, não apresentando elevação desses valores com a buprenorfina. Concluiu-se que não foi possível verificar a superioridade da neuroleptoanalgesia em relação ao uso dos fármacos isoladamente.

The antinociceptive effects of buprenorphine have been reported in dogs and cats. This study evaluated changes in the mechanical nociceptive threshold and the sedative effects of buprenorphine, acepromazine and its combination in cats, determined by the same observer using a nociceptive threshold testing device and DIVAS, respectively. Eight animals were previously conditioned to the procedures. After four baseline measurements, 0.02mg kg-1 of buprenorphine, 0.06mg.kg-1 of acepromazine, or 0.01mg kg-1 of buprenorphine with 0.03mg kg-1 of acepromazine were administered intramuscularly in a blinded and experimental study using a Latin square design within a one week interval between treatments. The antinociceptive and sedative effects were evaluated at 15, 30, 45 minutes and 1, 2, 3, 4, 6, 8 and 12 hours post treatment. The nociceptive threshold increased significantly only after the combination buprenorphine-acepromazine (between 45 minutes and 1 hour). Regarding sedation, the use of acepromazine and the combination of both were associated with significantly higher DIVAS values from 15 minutes to 4 hours and 15 minutes to 3 hours post treatment, respectively. No increase in these values was noted with the use of buprenorphine. It was concluded that it could not be verified the superiority of neuroleptanalgesia over the use of drugs alone.

Efeitos antinociceptivos e sedativos da buprenorfina, da acepromazina ou da associação buprenorfina e acepromazina em gatos

The antinociceptive effects of buprenorphine have been reported in dogs and cats. This study evaluated changes in the mechanical nociceptive threshold and the sedative effects of buprenorphine, acepromazine and its combination in cats, determined by the same observer using a nociceptive threshold testing device and DIVAS, respectively. Eight animals were previously conditioned to the procedures. After four baseline measurements, 0.02mg kg-1 of buprenorphine, 0.06mg.kg-1 of acepromazine, or 0.01mg kg-1 of buprenorphine with 0.03mg kg-1 of acepromazine were administered intramuscularly in a blinded and experimental study using a Latin square design within a one week interval between treatments. The antinociceptive and sedative effects were evaluated at 15, 30, 45 minutes and 1, 2, 3, 4, 6, 8 and 12 hours post treatment. The nociceptive threshold increased significantly only after the combination buprenorphine-acepromazine (between 45 minutes and 1 hour). Regarding sedation, the use of acepromazine and the combination of both were associated with significantly higher DIVAS values from 15 minutes to 4 hours and 15 minutes to 3 hours post treatment, respectively. No increase in these values was noted with the use of buprenorphine. It was concluded that it could not be verified the superiority of neuroleptanalgesia over the use of drugs alone

O efeito antinociceptivo da buprenorfina tem sido relatado em cães e gatos. No presente estudo, avaliou-se o limiar nociceptivo mecânico em felinos tratados com buprenorfina, acepromazina ou ambas associadas e foram comparados os efeitos antinociceptivos e sedativos da associação em relação ao uso isolado desses fármacos determinados pelo mesmo observador, por meio de analgesiômetro e da escala analógica visual dinâmica interativa (DIVAS), respectivamente. Os oito animais empregados no estudo foram previamente familiarizados com os procedimentos utilizados. Após quatro mensurações basais, foram administrados, por via intramuscular, 0,02mg kg-1 de buprenorfina, 0,06mg kg-1 de acepromazina ou 0,01mg kg-1 de buprenorfina associada a 0,03mg kg-1 de acepromazina, em um estudo cego, com delineamento em quadrado latino e tratamento semanal. Os efeitos antinociceptivos e sedativos foram avaliados aos 15, 30, 45 minutos e uma, duas, três, quatro, seis, oito e 12 horas após a administração do tratamento. O limiar nociceptivo mecânico se elevou significativamente apenas no grupo tratado com a associação buprenorfina-acepromazina (entre 45 minutos e uma hora). Em relação à sedação, nos grupos tratados com acepromazina e com a associação, os valores da DIVAS foram significativamente maiores, respectivamente, de 15 minutos até quatro horas e de 15 minutos até três horas pós-tratamento, não apresentando elevação desses valores com a buprenorfina. Concluiu-se que não foi possível verificar a superioridade da neuroleptoanalgesia em relação ao uso dos fármacos isoladamente.

Efeitos antinociceptivos e sedativos da buprenorfina, da acepromazina ou da associação buprenorfina e acepromazina em gatos

The antinociceptive effects of buprenorphine have been reported in dogs and cats. This study evaluated changes in the mechanical nociceptive threshold and the sedative effects of buprenorphine, acepromazine and its combination in cats, determined by the same observer using a nociceptive threshold testing device and DIVAS, respectively. Eight animals were previously conditioned to the procedures. After four baseline measurements, 0.02mg kg-1 of buprenorphine, 0.06mg.kg-1 of acepromazine, or 0.01mg kg-1 of buprenorphine with 0.03mg kg-1 of acepromazine were administered intramuscularly in a blinded and experimental study using a Latin square design within a one week interval between treatments. The antinociceptive and sedative effects were evaluated at 15, 30, 45 minutes and 1, 2, 3, 4, 6, 8 and 12 hours post treatment. The nociceptive threshold increased significantly only after the combination buprenorphine-acepromazine (between 45 minutes and 1 hour). Regarding sedation, the use of acepromazine and the combination of both were associated with significantly higher DIVAS values from 15 minutes to 4 hours and 15 minutes to 3 hours post treatment, respectively. No increase in these values was noted with the use of buprenorphine. It was concluded that it could not be verified the superiority of neuroleptanalgesia over the use of drugs alone

O efeito antinociceptivo da buprenorfina tem sido relatado em cães e gatos. No presente estudo, avaliou-se o limiar nociceptivo mecânico em felinos tratados com buprenorfina, acepromazina ou ambas associadas e foram comparados os efeitos antinociceptivos e sedativos da associação em relação ao uso isolado desses fármacos determinados pelo mesmo observador, por meio de analgesiômetro e da escala analógica visual dinâmica interativa (DIVAS), respectivamente. Os oito animais empregados no estudo foram previamente familiarizados com os procedimentos utilizados. Após quatro mensurações basais, foram administrados, por via intramuscular, 0,02mg kg-1 de buprenorfina, 0,06mg kg-1 de acepromazina ou 0,01mg kg-1 de buprenorfina associada a 0,03mg kg-1 de acepromazina, em um estudo cego, com delineamento em quadrado latino e tratamento semanal. Os efeitos antinociceptivos e sedativos foram avaliados aos 15, 30, 45 minutos e uma, duas, três, quatro, seis, oito e 12 horas após a administração do tratamento. O limiar nociceptivo mecânico se elevou significativamente apenas no grupo tratado com a associação buprenorfina-acepromazina (entre 45 minutos e uma hora). Em relação à sedação, nos grupos tratados com acepromazina e com a associação, os valores da DIVAS foram significativamente maiores, respectivamente, de 15 minutos até quatro horas e de 15 minutos até três horas pós-tratamento, não apresentando elevação desses valores com a buprenorfina. Concluiu-se que não foi possível verificar a superioridade da neuroleptoanalgesia em relação ao uso dos fármacos isoladamente.

Efeitos antinociceptivos e sedativos da buprenorfina, da acepromazina ou da associação buprenorfina e acepromazina em gatos

The antinociceptive effects of buprenorphine have been reported in dogs and cats. This study evaluated changes in the mechanical nociceptive threshold and the sedative effects of buprenorphine, acepromazine and its combination in cats, determined by the same observer using a nociceptive threshold testing device and DIVAS, respectively. Eight animals were previously conditioned to the procedures. After four baseline measurements, 0.02mg kg-1 of buprenorphine, 0.06mg.kg-1 of acepromazine, or 0.01mg kg-1 of buprenorphine with 0.03mg kg-1 of acepromazine were administered intramuscularly in a blinded and experimental study using a Latin square design within a one week interval between treatments. The antinociceptive and sedative effects were evaluated at 15, 30, 45 minutes and 1, 2, 3, 4, 6, 8 and 12 hours post treatment. The nociceptive threshold increased significantly only after the combination buprenorphine-acepromazine (between 45 minutes and 1 hour). Regarding sedation, the use of acepromazine and the combination of both were associated with significantly higher DIVAS values from 15 minutes to 4 hours and 15 minutes to 3 hours post treatment, respectively. No increase in these values was noted with the use of buprenorphine. It was concluded that it could not be verified the superiority of neuroleptanalgesia over the use of drugs alone

O efeito antinociceptivo da buprenorfina tem sido relatado em cães e gatos. No presente estudo, avaliou-se o limiar nociceptivo mecânico em felinos tratados com buprenorfina, acepromazina ou ambas associadas e foram comparados os efeitos antinociceptivos e sedativos da associação em relação ao uso isolado desses fármacos determinados pelo mesmo observador, por meio de analgesiômetro e da escala analógica visual dinâmica interativa (DIVAS), respectivamente. Os oito animais empregados no estudo foram previamente familiarizados com os procedimentos utilizados. Após quatro mensurações basais, foram administrados, por via intramuscular, 0,02mg kg-1 de buprenorfina, 0,06mg kg-1 de acepromazina ou 0,01mg kg-1 de buprenorfina associada a 0,03mg kg-1 de acepromazina, em um estudo cego, com delineamento em quadrado latino e tratamento semanal. Os efeitos antinociceptivos e sedativos foram avaliados aos 15, 30, 45 minutos e uma, duas, três, quatro, seis, oito e 12 horas após a administração do tratamento. O limiar nociceptivo mecânico se elevou significativamente apenas no grupo tratado com a associação buprenorfina-acepromazina (entre 45 minutos e uma hora). Em relação à sedação, nos grupos tratados com acepromazina e com a associação, os valores da DIVAS foram significativamente maiores, respectivamente, de 15 minutos até quatro horas e de 15 minutos até três horas pós-tratamento, não apresentando elevação desses valores com a buprenorfina. Concluiu-se que não foi possível verificar a superioridade da neuroleptoanalgesia em relação ao uso dos fármacos isoladamente.