The impact of acepromazine on the efficacy of crystalloid,dextran or ephedrine treatment in hypotensive dogs under isoflurane anesthesia

ObjectiveTo determine the impact of acepromazine on the cardiovascular responses to three treatments for hypotension in dogs during deep isoflurane anesthesia.Study designProspective blinded randomized cross-over experimental design.AnimalsSix adult (2.5 ± 0.5 year old) healthy mixed breed dogs (24.2 ± 7.6 kg).MethodsAnesthesia was induced with propofol (4–6 mg kg^?1, IV) and maintained with isoflurane. Each dog received six treatments separated by at least 5 days. Once instrumented, dogs randomly received acepromazine (0.05 mg kg^?1) (Ace) or saline (equal volume) (Sal) IV and end-tidal isoflurane (e′Iso) was adjusted to achieve hypotension, defined as a mean blood pressure between 45 and 50 mmHg. Dogs randomly received dextran (D) (7 mL kg^?1) or lactated Ringer's (LR) (20 mL kg^?1) over 14 minutes, or ephedrine (Eph) (0.1 mg kg^?1 followed by 10 μg kg^?1 minute^?1) throughout the study. Measurements were taken at baseline, 5, 10, 15, 20, 30, and 40 minutes. Data were analyzed with a Latin Square in two factors (Ace/Sal and treatment) for repeated measures, with further comparisons if appropriate (p < 0.05).Resultse′Iso producing hypotension was significantly less following Ace (2.07 ± 0.23%) than Sal (2.43 ± 0.23%). No improvement in cardiac output (CO) was observed with D or LR. LR initially intensified hypotension with a significant reduction in SVR, while D caused a minor improvement in ABP. Eph produced a significant increase in ABP, CO, hemoglobin, oxygen content and delivery. Pre-treatment with Ace minimized ABP improvements with all treatments.Conclusions and clinical relevanceAcepromazine (0.05 mg kg^?1 IV) enhanced the hypotensive effect of isoflurane, although it maintained CO. Administration of LR significantly worsens ABP initially by further vasodilation. D caused minimal improvement in ABP. At the infusion studied, Eph effectively countered the cardiovascular depression produced by deep isoflurane anesthesia, but extremes in ABP associated with initial vasoconstriction prevent our recommendation at this dose.     

Administration of acepromazine maleate to 31 dogs with a history of seizures

Objective: To retrospectively evaluate the incidence of seizures in dogs presenting with a history of seizures that were treated with acepromazine (ACE) during hospitalization. Design: Retrospective study. Setting: Privately owned emergency and referral hospital. Animals: Thirty‐one client‐owned dogs. Interventions: Administration of ACE. Measurements and main results: The medical records from dogs with an acute or chronic seizure history that received ACE were reviewed. Factors evaluated included presenting complaint, seizure history, ACE dosage, duration of observation, seizure activity, and other medications used. Thirty‐one dogs qualified for the study: 20 males and 11 females. Age range was 3 months to 14.9 years. Presenting complaint was seizure in 28/31 dogs. There was a prior history of seizures in 22/31 dogs, and 15/22 were currently on antiseizure medication. ACE was given 1–5 times per dog. Mean ACE dose was 0.029 mg/kg IV (range: 0.008–0.057 mg/kg; n=46), 0.036 mg/kg IM (range: 0.017–0.059 mg/kg; n=14), 0.53 mg/kg PO (n=2). Twenty‐seven dogs did not seizure after administration of ACE within the observation period (mean: 16.4 hours, range: 0.25–66 hours). Twenty‐five dogs received antiseizure medication before ACE. Eight seizure episodes occurred in 4 dogs (all of whom presented for seizures) within 0.3–10 hours after ACE administration. Conclusions: There was no observed correlation between ACE administration in dogs with a seizure history and the recurrence of seizure activity during hospitalization. The time from ACE administration to seizure activity was greater than expected for measurable effects to be seen in 1 dog (10 hour). Further studies with a larger group and alternative ACE doses are needed to more thoroughly evaluate the safety of short‐term ACE use in dogs with a seizure history.     

Effects of intravenous acepromazine and butorphanol on propofol dosage for induction of anesthesia in healthy Beagle dogs

ObjectiveTo determine the effects of intravenous (IV) premedication with acepromazine, butorphanol or their combination, on the propofol anesthetic induction dosage in dogs.Study designProspective, blinded, Latin square design.AnimalsA total of three male and three female, healthy Beagle dogs, aged 3.79 ± 0.02 years, weighing 10.6 ± 1.1 kg, mean ± standard deviation.MethodsEach dog was assigned to one of six IV treatments weekly: 0.9% saline (treatment SAL), low-dose acepromazine (0.02 mg kg^–1; treatment LDA), high-dose acepromazine (0.04 mg kg^–1; treatment HDA), low-dose butorphanol (0.2 mg kg^–1; treatment LDB), high-dose butorphanol (0.4 mg kg^–1; treatment HDB); and a combination of acepromazine (0.02 mg kg^–1) with butorphanol (0.2 mg kg^–1; treatment ABC). Physiologic variables and sedation scores were collected at baseline and 10 minutes after premedication. Then propofol was administered at 1 mg kg^–1 IV over 15 seconds, followed by boluses (0.5 mg kg^–1 over 5 seconds) every 15 seconds until intubation. Propofol dose, physiologic variables, recovery time, recovery score and adverse effects were monitored and recorded. Data were analyzed using mixed-effects anova (p < 0.05).ResultsPropofol dosage was lower in all treatments than in treatment SAL (4.4 ± 0.5 mg kg^–1); the largest decrease was recorded in treatment ABC (1.7 ± 0.3 mg kg^–1). Post induction mean arterial pressures (MAPs) were lower than baseline values of treatments LDA, HDA and ABC. Apnea and hypotension (MAP < 60 mmHg) developed in some dogs in all treatments with the greatest incidence of hypotension in treatment ABC (4/6 dogs).Conclusions and clinical relevanceAlthough the largest decrease in propofol dosage required for intubation was after IV premedication with acepromazine and butorphanol, hypotension and apnea still occurred.     

Two doses of dexmedetomidine in combination with buprenorphine for premedication in dogs; a comparison with acepromazine and buprenorphine

ObjectiveTo assess as premedicants, the sedative, cardiorespiratory and propofol-sparing effects in dogs of dexmedetomidine and buprenorphine compared to acepromazine and buprenorphine.Study designProspective, randomised, blinded clinical studyAnimalsSixty healthy dogs (ASA grades I/II). Mean (SD) body mass 28.0 ± 9.1 kg, and mean age 3.4 ± 2.3 years.MethodsDogs were allocated randomly to receive 15 μg kg^?1 buprenorphine combined with either 30 μg kg^?1 acepromazine (group 1), 62.5 μg m^?2 dexmedetomidine (group 2), or 125 μg m^?2 dexmedetomidine (group 3) intramuscularly. After 30 minutes, anaesthesia was induced using a propofol target controlled infusion. Heart rate, respiratory rate, and oscillometric arterial blood pressure were recorded prior to induction, at endotracheal intubation and at 3 and 5 minutes post-intubation. Induction quality and pre-induction sedation were scored on 4 point scales. Propofol target required for endotracheal intubation was recorded. Data were analysed using Chi-squared tests, Kruskal-Wallis, one way and general linear model anova (p < 0.05).ResultsAge was significantly lower in group 1 (1.0 (1.0–3.8) years) than group 2 (5.0 (2.0–7.0) years), (median, (IQR)). There were no significant differences in sedation or quality of induction between groups. After premedication, heart rate was significantly lower and arterial blood pressures higher in groups 2 and 3 than group 1, but there was no significant difference between groups 2 and 3. Propofol targets were significantly lower in group 3 (1.5 (1.0–2.5) μg mL^?1) than group 1 (2.5 (2.0–3.0) μg mL^?1); no significant differences existed between group 2 (2.0 (1.5–2.5) μg mL^?1) and the other groups (median, (interquartile range)).Conclusions and Clinical relevanceWhen administered with buprenorphine, at these doses, dexmedetomidine had no advantages in terms of sedation and induction quality over acepromazine. Both doses of dexmedetomidine produced characteristic cardiovascular and respiratory effects of a similar magnitude.     

Contemporary use of acepromazine in the anaesthetic management of male horses and ponies: a retrospective study and opinion poll

Reason for performing study: Current use of acepromazine in the anaesthetic management of male horses and ponies and associated risks are largely unknown. Objectives: To explore anaesthetic acepromazine use and related adverse effects in the male horse. Methods: Of 8533 anaesthetised horses and ponies medical records of male animals treated perianaesthetically with acepromazine were reviewed. Demographic data, time and dose of acepromazine administration, co‐administered drugs, quality of induction and recovery from anaesthesia, arterial blood pressures, and occurrence of penile dysfunction were recorded. Practising ACVA and ECVAA diplomates were polled on the use of acepromazine and its effects on blood pressure and penile dysfunction in the equine. Results: Of all animals, 12% females and 11% males (n = 575 including 42% stallions) received perianaesthetic acepromazine, predominantly for premedication. Anaesthetic induction was smooth in 566 animals. Lowest mean arterial pressures averaged 65 ± 9 mmHg. Recovery was good or very good in 70% of all animals and 74% stood after 1–2 attempts. In 14 horses (2.4%; 7 stallions, 7 geldings), penile prolapse occurred for 0.5–4 h and in one stallion (0.2%) for >12 but <18 h post recovery. Most surveyed anaesthesiologists use acepromazine in stallions (occasionally 63%; frequently 17%) but more frequently in geldings (occasionally 34%; frequently 59%) and mares (occasionally 38%; frequently 59%), primarily for premedication with other sedatives and analgesics. Persistent intraoperative hypotension was not frequently reported. Only 5% of surveyed anaesthesiologists recall penile prolapse post acepromazine administration lasting for >12 h and only one recalls 3 cases of irreversible penile prolapse in 20 years of anaesthesia practice. Conclusions and potential relevance: The extremely low risk of permanent penile dysfunction (≤1 in 10,000 cases) does not justify more restricted use of acepromazine in the intact male vs. geldings and mares.     

Comparison between dexmedetomidine and acepromazine in combination with methadone for premedication in brachycephalic dogs undergoing surgery for brachycephalic obstructive airway syndrome

ObjectiveTo compare dexmedetomidine with acepromazine for premedication combined with methadone in dogs undergoing brachycephalic obstructive airway syndrome (BOAS) surgery.Study designRandomized, blinded clinical study.AnimalsA group of 40 dogs weighing mean (± standard deviation) 10.5 ± 6 kg, aged 2.6 ± 1.9 years.MethodsDogs received either acepromazine 20 μg kg^–1 (group A) or dexmedetomidine 2 μg kg^–1 (group D) intramuscularly with methadone 0.3 mg kg^–1. Anaesthesia was induced with propofol and maintained with sevoflurane. Sedation (0–18), induction (0–6) and recovery (0–5) qualities were scored. Propofol dose, hypotension incidence, mechanical ventilation requirement, extubation time, additional sedation, oxygen supplementation, regurgitation and emergency intubation following premedication or during recovery were recorded. Data were analysed using t tests, Mann-Whitney U or Chi-square tests.ResultsGroup A dogs were less sedated [median (range): 1.5 (0–12)] than group D [5 (1–18)] (p = 0.021) and required more propofol [3.5 (1–7) versus 2.4 (1–8) mg kg^–1; p = 0.018]. Induction scores [group A: 5 (4–5); group D 5 (3–5)] (p = 0.989), recovery scores [group A 5 (4–5); group D 5(3–5)](p = 0.738) and anaesthesia duration [group A:93 (50–170); group D 96 (54–263) minutes] (p = 0.758) were similar between groups. Time to extubation was longer in group A 12.5 (3-35) versus group D 5.5 (0–15) minutes; (p = 0.005). During recovery, two dogs required emergency intubation (p > 0.99) and five dogs required additional sedation (p > 0.99). Oxygen supplementation was required in 16 and 12 dogs in group A and D, respectively (p = 0.167); no dogs in group A and one dog in group D regurgitated (p = 0.311).Conclusions and clinical relevanceDexmedetomidine 2 μg kg^–1 produces more sedation but similar recovery quality to acepromazine 20 μg kg^–1 combined with methadone in dogs undergoing BOAS surgery.     

Comparison of the effects of alfaxalone and propofol with acepromazine,butorphanol and/or doxapram on laryngeal motion and quality of examination in dogs

Objective

To compare the effects of alfaxalone and propofol, with and without acepromazine and butorphanol followed by doxapram, on laryngeal motion and quality of laryngeal examination in dogs.

Anesthesia in Caspian ponies

ObjectiveTo evaluate some of the clinical and laboratory parameters following diazepam–acepromazine, thiopental, and halothane anesthesia in Caspian ponies.Study designProspective experimental trial.AnimalsSix healthy Caspian ponies of both sexes, aged 11 ± 3 years and weighing 318 ± 71 kg.MethodsThe ponies were pre-medicated with diazepam (0.2 mg kg⁻¹) and acepromazine (0.05 mg kg⁻¹) IV. Sodium thiopental 5% was administered IV, 10 minutes later and anesthesia was maintained with halothane in oxygen for 1 hour. Heart and respiratory rates, mean arterial blood pressure, cardiac rhythm, and signs of anesthetic depth were monitored during anesthesia. Hematological and serum biochemical parameters were evaluated before anesthesia and at 1, 2, 3, 24, 48, 72, and 96 hours. Urine specific gravity and cytology were evaluated at the same intervals following anesthesia. Parametric data were analyzed using repeated measures anova.ResultsConsiderable sedation/tranquilization without excitement was achieved following pre-medication. Heart rate significantly increased and mild hypotension occurred during anesthesia. Sinus arrhythmia and second degree AV block occurred in five horses. Respiratory rate decreased during anesthesia, with an accompanying respiratory acidosis. Body temperature also decreased. Recovery was scored ‘good’ in four horses and ‘satisfactory’ in the other two. Blood urea nitrogen concentration was significantly increased at 1–3 hours post-anesthesia. Blood glucose was significantly increased at 48, 72, and 96 hours, and creatine kinase and aspartate aminotransferase were significantly increased at 24 and 48 hours post-anesthesia.Conclusion and clinical relevance This simple anesthetic protocol can be used in Caspian ponies and an acceptable anesthetic with a reasonable recovery can be expected.     

The effects of detomidine, romifidine or acepromazine on echocardiographic measurements and cardiac function in normal horses

OBJECTIVE: To evaluate by echo- and electrocardiography the cardiac effects of sedation with detomidine hydrochloride, romifidine hydrochloride or acepromazine maleate in horses. STUDY DESIGN: An experimental study using a cross-over design without randomization. ANIMALS: Eight clinically normal Standardbred trotters. MATERIALS AND METHODS: Echocardiographic examinations (two-dimensional, guided M-mode and colour Doppler) were recorded on five different days. Heart rate (HR) and standard limb lead electrocardiograms were also obtained. Subsequently, horses were sedated with detomidine (0.01 mg kg(-1)), romifidine (0.04 mg kg(-1)) or acepromazine (0.1 mg kg(-1)) administered intravenously and all examinations repeated. RESULTS: Heart rate before treatment with the three drugs did not differ significantly (p = 0.98). Both detomidine and romifidine induced a significant decrease (p < 0.001) in HR during the first 25 minutes after sedation; while acepromazine had a varying effect on HR. For detomidine, there was a significant increase in LVIDd (left ventricular internal diameter in diastole; p = 0.034) and LVIDs (left ventricular internal diameter in systole; p < 0.001). In addition, a significant decrease was found in IVSs (the interventricular septum in systole; p < 0.001), LVFWs (the left ventricular free wall in systole; p = 0.002) and FS% (fractional shortening; p < 0.001). The frequency of pulmonary regurgitation was increased significantly (p < 0.001). Romifidine induced a significant increase in LVIDs (p < 0.001) and a significant decrease in IVSs (p < 0.001) and FS% (p = 0.002). Acepromazine had no significant effect upon any of the measured values. CONCLUSIONS: and clinical relevance The results indicate that sedation of horses with detomidine and to a lesser extent romifidine at the doses given in this study has a significant effect on heart function, echocardiographic measurements of heart dimensions and the occurrence of valvular regurgitation. Although the clinical significance of these results may be minimal, the potential effects of sedative drugs should be taken into account when echocardiographic variables are interpreted in clinical cases.