Hemodynamic effects of incremental doses of acepromazine in isoflurane-anesthetized dogs.

OBJECTIVE: To evaluate the effects of incremental doses of acepromazine on hemodynamics in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: Healthy, adult, mixed-breed dogs (two male and four female) weighing 16.8 ± 5.1 kg (mean ± standard deviation). METHODS: Dogs were anesthetized with propofol (7 mg kg-1) intravenously (IV) and isoflurane. Thermodilution and arterial catheters were placed for hemodynamic monitoring and arterial blood sampling for blood gas analysis. Baseline measurements were performed with stable expired concentration of isoflurane (Fe'Iso) at 1.8%. Each dog was then administered four incremental acepromazine injections (10, 15, 25 and 50 µg kg-1) IV, and measurements were repeated 20 minutes after each acepromazine injection with Fe'Iso decreased to 1.2%. The four acepromazine injections resulted in cumulative doses of 10, 25, 50 and 100 µg kg-1 (time points ACP10, ACP25, ACP50 and ACP100, respectively). RESULTS: Compared with baseline, cardiac index (CI) increased significantly by 34%, whereas systemic vascular resistance index (SVRI) decreased by 25% at ACP50 and ACP100. Arterial oxygen content (CaO2) was significantly lower than baseline after all acepromazine injections (maximum decreases of 11%) and was lower at ACP50 and ACP100 than at ACP10. No significant change was found in heart rate, stroke index, oxygen delivery index and systolic, mean and diastolic blood pressures. Hypotension (mean arterial pressure < 60 mmHg) was observed in one dog at baseline, ACP10, ACP25 and ACP100, and in two dogs at ACP50. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with isoflurane alone, anesthesia with acepromazine-isoflurane resulted in increased CI and decreased SVRI and CaO2 values. These effects were dose-related, being more pronounced at ACP50 and ACP100. Under the conditions of this study, acepromazine administration did not change blood pressure.

Hemodynamic, respiratory and sedative effects of progressively increasing doses of acepromazine in conscious dogs.

OBJECTIVE: To evaluate the effects of progressively increasing doses of acepromazine on cardiopulmonary variables and sedation in conscious dogs. STUDY DESIGN: Prospective, experimental study. ANIMALS: A group of six healthy, adult, mixed-breed dogs weighing 16.5 ± 5.0 kg (mean ± standard deviation). METHODS: Dogs were instrumented with thermodilution and arterial catheters for evaluation of hemodynamics and arterial blood gases. On a single occasion, acepromazine was administered intravenously to each dog at 10, 15, 25 and 50 µg kg-1 at 20 minute intervals, resulting in cumulative acepromazine doses of 10 µg kg-1 (ACP10), 25 µg kg-1 (ACP25), 50 µg kg-1 (ACP50) and 100 µg kg-1 (ACP100). Hemodynamic data and sedation scores were recorded before (baseline) and 20 minutes after each acepromazine dose. RESULTS: Compared with baseline, all acepromazine doses significantly decreased stroke index (SI), mean arterial pressure (MAP) and arterial oxygen content (CaO2) with maximum decreases of 16%, 17% and 21%, respectively. Cardiac index (CI) decreased by up to 19% but not significantly. Decreases of 26-38% were recorded for oxygen delivery index (DO2I), with significant differences for ACP50 and ACP100. Systemic vascular resistance index (SVRI) and heart rate did not change significantly. No significant difference was found among acepromazine doses for hemodynamic data. After ACP10, mild sedation was observed in five/six dogs and moderate sedation in one/six dogs, whereas after ACP25, ACP50 and ACP100, moderate sedation was observed in five/six or six/six dogs. CONCLUSIONS AND CLINICAL RELEVANCE: In conscious dogs, acepromazine decreased MAP, SI, CaO2 and DO2I, but no significant dose effect was detected. SVRI was not significantly changed, suggesting that the reduction in MAP resulted from decreased CI. The ACP25, ACP50 and ACP100 doses resulted in moderate sedation in most dogs; ACP10 resulted in only mild sedation.

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.

Tramadol does not enhance sedation induced by acepromazine in dogs.

The sedative effect of acepromazine combined with 2 doses of tramadol [3 and 5 mg/kg body weight (BW)] was compared with the sedative effect of acepromazine alone in dogs and the effects of each sedative protocol on cardiorespiratory variables were examined. This was a prospective, randomized, blinded, crossover study. Each of 6 dogs received 3 treatments at 1-week intervals. During all anesthetic episodes, dogs received 0.05 mg/kg BW acepromazine. Approximately 25 min later, dogs were given physiological saline (control) or tramadol [3 mg/kg BW (TR3) or 5 mg/kg BW (TR5)]. All drugs were administered intravenously. Variables evaluated included heart rate (HR), respiratory rate (RR), systolic, mean, and diastolic blood pressures (SAP, MAP, and DAP), and sedation [by use of a simple descriptive scale (SDS, range: 0 to 3) and a numeric rating scale (NRS, range: 0 to 10)]. Variables were recorded 25 min after acepromazine and for 80 min after saline or tramadol. Acepromazine administration resulted in mild sedation in most dogs and decreased RR, SAP, MAP, and DAP in all treatments. Tramadol administration did not significantly increase SDS or NRS scores compared to acepromazine alone. The only exception to this rule was observed at 20 min after TR3, when NRS was higher in this group than in the control treatment. Administration of tramadol (TR3 and TR5) decreased HR. Under the conditions of this study, sedation induced by acepromazine with tramadol was similar to that of acepromazine alone. The main adverse effects of the combination were a decrease in blood pressure and HR, without clinical significance.

L'effet sédatif de l'acépromazine combiné à deux doses de tramadol [3 et 5 mg/kg de poids corporel (PC)] a été comparé à l'effet sédatif de l'acépromazine seul chez des chiens et les effets de chaque protocole de sédation sur des variables cardio-respiratoires ont été examinés. Il s'agissait d'une étude prospective croisée, randomisée, réalisée à l'aveugle. Chacun des six chiens a reçu trois traitements à des intervalles de 1 semaine. Durant tous les épisodes anesthétiques, les chiens ont reçu 0,05 mg/kg PC d'acépromazine. Environ 25 min plus tard, les chiens ont reçu de la saline physiologique (témoin) ou du tramadol [3 mg/kg PC (TR3) ou 5 mg/kg PC (TR5)]. Toutes les drogues étaient administrées par voie intraveineuse. Les variables évaluées incluaient le rythme cardiaque (RC), le rythme respiratoire (RR), les pressions sanguines systolique, moyenne, et diastolique (PSS, PSM, et PSD), et la sédation [en utilisant une échelle descriptive simple (EDS, écart : 0 à 3) et une échelle de gradation numérique (EGN, écart : 0 à 10)]. Les variables ont été enregistrées 25 min après l'acépromazine et pendant 80 min après l'administration de saline ou de tramadol. L'administration d'acépromazine a résulté en une légère sédation chez la plupart des chiens et on nota une diminution de RR, PSS, PSM, et PSD avec tous les traitements. L'administration de tramadol ne fit pas augmenter de manière significative les pointages EDS et EGN lorsque comparée à l'acépromazine seul. La seule exception à cette règle a été observée à 20 min après TR3, alors que l'EGN était plus élevée dans ce groupe comparativement au témoin. L'administration de tramadol (TR3 et TR5) entraîna une diminution du RC. Dans les conditions de la présente étude, la sédation induite par l'acépromazine avec du tramadol était similaire à celle de l'acépromazine seul. Les principaux effets adverses de la combinaison étaient une diminution de la pression sanguine et du RC, mais sans signification clinique.(Traduit par Docteur Serge Messier).