Influence of fentanyl, medetomidine-fentanyl or acepromazine-fentanyl premedication on oesophageal and rectal temperature in dogs under anaesthesia.

OBJECTIVE: To compare changes in oesophageal (T-Oeso) and rectal (T-Rec) temperature in dogs during general anaesthesia and premedicated with fentanyl, medetomidine-fentanyl or acepromazine-fentanyl. STUDY DESIGN: Prospective, randomized, blind clinical study. ANIMALS: A total of 120 healthy dogs, aged 2-10 years and weighing 5-20 kg. METHODS: Dogs were randomly allocated to one of three groups. Animals of F group were premedicated with fentanyl (0.01 mg kg-1), MF group with medetomidine (0.005 mg kg-1) and fentanyl (0.01 mg kg-1) and AF group with acepromazine (0.01 mg kg-1) and fentanyl (0.01 mg kg-1). Anaesthesia was induced with propofol and maintained with isoflurane in oxygen-air mixture. Fentanyl was administered continuously (0.01 mg kg-1 hour-1). The T-Oeso, T-Rec and ambient temperatures were recorded after induction (T0) and subsequently at 10 minute intervals for 60 minutes (T10-T60). Data were analysed using anova or their non-parametric equivalents (p < 0.05). RESULTS: Median T-Oeso was significantly higher in MF group between T0-T20 compared with other groups. Median T-Oeso significantly decreased in F group from 38.0 °C (T0) to 37.4 °C (T30), 37.1 °C (T40), 36.9 °C (T50) and 36.6 °C (T60), in MF group from 38.3 °C (T0) to 37.7 °C (T30), 37.5 °C (T40), 37.2 °C (T50) and 37.1 °C (T60) and in AF group from 37.7 °C (T0) to 37.3 °C (T40), 37.2 °C (T50) and 37.1 °C (T60). The T-Rec significantly decreased in F group from 38.0 °C (T0) to 37.4 °C (T40), 37.2 °C (T50) and 36.9 °C (T60), in MF group from 38.3 °C (T0) to 37.5 °C (T50) and 37.4 °C (T60) and in AF group from 38.2 °C (T0) to 37.6 °C (T40), 37.5 °C (T50) and 37.4 °C (T60). CONCLUSIONS AND CLINICAL RELEVANCE: Premedication with fentanyl, medetomidine-fentanyl or acepromazine-fentanyl in the doses used decreased the T-Oeso and T-Rec. The T-Oeso at the beginning of anaesthesia was higher after premedication with medetomidine-fentanyl. However, this difference was not clinically significant.

Sedative and cardiorespiratory effects of dexmedetomidine alone or combined with acepromazine in healthy cats.

The purpose of this study was to assess sedation, emesis and cardiovascular effects of dexmedetomidine alone or combined with acepromazine in healthy cats. Fourteen male cats aged 0.9 ± 0.5 years and weighing 3.7 ± 0.7 kg were randomly assigned to one of two experimental groups: GD, dexmedetomidine 5 µg/kg; and GDA, dexmedetomidine 5 µg/kg with acepromazine 0.03 mg/kg, all intramuscularly. Measurements were recorded at baseline, at 20 minutes and then at 10-minute intervals following sedation and included heart rate (HR), respiratory rate (FR), systolic arterial pressure (SAP), rectal temperature (RT), number of episodes of emesis and sedation score (0-4). Data were compared using ANOVA for repeated measures followed by Sídák and Dunnet test. Sedation scores were compared between groups at T20 using Mann-Whitney test. Significance was considered when P <0.05. At T20, HR was significantly lower in GDA (99 ± 14 beats/min) compared with GD (133 ± 19 beats/min) and SAP was significantly lower in both groups compared with baseline (126 ± 14 vs. 148 ± 26 and 111 ± 13 vs. 144 ± 17 mmHg in GD and GDA, respectively). Duration of sedation was similar between groups, although sedation scores differed significantly at T20, with 1 (0-4) in GD and 4 (4-4) in GDA. More episodes of emesis were recorded in GD compared with GDA. The combination of dexmedetomidine and acepromazine produced more profound sedation with faster onset and lower incidence of emesis compared with dexmedetomidine alone in healthy cats.

Phenylephrine and norepinephrine increase blood pressure through opposing physiologic mechanisms in isoflurane-anesthetized dogs receiving acepromazine.

OBJECTIVE: To elucidate the cardiovascular effects of escalating doses of phenylephrine and norepinephrine in dogs receiving acepromazine and isoflurane. ANIMALS: 8 beagles aged 1 to 2 years (7.4 to 11.2 kg). METHODS: All dogs received acepromazine 0.01 mg/kg, propofol 4 to 5 mg/kg, and isoflurane and were mechanically ventilated. Mean arterial pressure (MAP) from a femoral artery catheter and continuous electrocardiogram were recorded. Cardiac output (CO) was measured with transpulmonary thermodilution. Systemic vascular resistance (SVR), global end-diastolic volume (GEDV), and global ejection fraction (GEF) were subsequently calculated. Phenylephrine and norepinephrine were infused in random order at 0.07, 0.3, 0.7, and 1.0 µg/kg/min. All variables were measured after 15 minutes of each infusion rate. The effects of dose, agent, and their interaction on the change of each variable were evaluated with mixed-effect models. A P < .05 was used for significance. RESULTS: Atrial premature complexes occurred in 3 dogs during norepinephrine infusion at doses of 0.3, 0.7, and 1 µg/kg/min; no dysrhythmias were seen with phenylephrine administration. MAP increased during dose escalation (P < .0001) within each agent and did not differ between agents (P = .6). The decrease in HR was greater for phenylephrine (P < .0001). Phenylephrine decreased CO and GEF and increased GEDV and SVR (all P < .03). Norepinephrine decreased the SVR and increased CO, GEDV, and GEF (all P < .03). CLINICAL RELEVANCE: Our results confirm that phenylephrine increases arterial pressures mainly through vasoconstriction in acepromazine-premedicated dogs while norepinephrine, historically considered a vasopressor, does so primarily through an increase in inotropism.

Gabapentin, melatonin, and acepromazine combination prior to hospital visits decreased stress scores in aggressive and anxious dogs in a prospective clinical trial.

OBJECTIVE: To evaluate sedative and behavioral effects of a client-administered preappointment protocol with PO gabapentin and melatonin and oral-transmucosal acepromazine (GMA protocol). ANIMALS: 45 client-owned dogs between 1 and 12 years old that underwent standardize examinations between February and August 2021. METHODS: In this clinical trial, dogs with a history of anxiety, fearfulness, and/or aggression during hospital visits were assessed and videotaped before (baseline) and after administration of the GMA protocol. For the second visit, owners administered PO gabapentin (20 to 25 mg/kg) in the evening prior to the next visit and PO gabapentin (20 to 25 mg/kg), PO melatonin (3 to 5 mg/dog), and oral-transmucosal acepromazine (0.05 mg/kg) 90 to 120 minutes prior to the second appointment. Examinations were performed, and behavioral stress and sedation levels were evaluated with semiquantitative rating scales. Randomized videos were analyzed, and a paired t test was used to compare stress and sedation scores between baseline and GMA. A Pearson correlation coefficient was used to evaluate the effect of age on the scores. RESULTS: Stress scores were significantly lower after the GMA protocol, and sedation scores were significantly higher when compared to baseline (21.84 vs 27.11 and 1.39 vs 0.68, respectively). A significant correlation between increasing age and lower stress scores post-GMA and higher sedation scores post-GMA were observed. CLINICAL RELEVANCE: Preappointment administration of the GMA protocol reduced signs of stress, fear, and fear-based aggression during hospital visits and provided sedation in this dog population. This protocol could represent an adjunct tool for veterinarians to improve quality of care and reduce animal-related injury.

Effect of common sedation agents on feline splenic size determined via ultrasonography.

AIMS: To evaluate the effect of IM administration of three sedative drugs, acepromazine, alfaxalone and dexmedetomidine, in combination with morphine, on the size of the feline spleen using ultrasonography. METHODS: Twenty-four client-owned cats undergoing elective de-sexing or minor procedures were recruited for a focused ultrasonographic examination of the spleen prior to and at 10, 20 and 30 minutes following administration of one of three randomly assigned IM sedation protocols: 0.05 mg/kg acepromazine (ACE group), 3 mg/kg alfaxalone (ALF group), or 10 µg/kg dexmedetomidine (DEX group), in combination with 0.5 mg/kg morphine. B-mode images of the spleen were collected and measured following a standardised protocol. Cardiorespiratory parameters and sedation score were also recorded. Mean thickness of the head, body and tail of the spleen for each group at 10, 20 and 30 minutes after drug administration was compared to baseline. RESULTS: Mean splenic thickness increased over time in the ACE group (thickness of body at T0 = 8.9 (SE 2.1) mm and at T30 = 10.5 (SE 2.0) mm; p = 0.001) and the ALF group (thickness of body at T0 = 8.8 (SE 1.0) mm and at T30 = 10.3 (SE 1.7) mm; p = 0.022) but not in the DEX group (thickness of body at T0 = 8.6 mm (1.2) and at T30 = 8.9 mm (0.6); p = 0.67). Mean arterial blood pressure in the DEX group was significantly higher than in the other groups (p = 0.002). Sedation scores in the DEX group were consistently high for the entire period. However, the sedation score in the ACE group increased over 30 minutes (p = 0.007). Sedation score in the ALF group was highest at 10 minutes but gradually decreased over the following 20 minutes (p = 0.003). CONCLUSIONS: Sedation with IM dexmedetomidine and morphine did not change splenic size, whereas acepromazine or alfaxalone and morphine increased it regardless of the degree of sedation. CLINICAL RELEVANCE: Where splenomegaly is identified in a cat sedated with acepromazine or alfaxalone, the effects of the sedation protocol could be considered as a possible cause.

Ketamine-propofol for total intravenous anaesthesia in rabbits: a comparison of premedication with acepromazine-medetomidine, acepromazine-midazolam or acepromazine-morphine.

OBJECTIVE: To describe ketamine-propofol total intravenous anaesthesia (TIVA) following premedication with acepromazine and either medetomidine, midazolam or morphine in rabbits. STUDY DESIGN: Randomized, crossover experimental study. ANIMALS: A total of six healthy female New Zealand White rabbits (2.2 ± 0.3 kg). METHODS: Rabbits were anaesthetized on four occasions, each separated by 7 days: an intramuscular injection of saline alone (treatment Saline) or acepromazine (0.5 mg kg-1) in combination with medetomidine (0.1 mg kg-1), midazolam (1 mg kg-1) or morphine (1 mg kg-1), treatments AME, AMI or AMO, respectively, in random order. Anaesthesia was induced and maintained with a mixture containing ketamine (5 mg mL-1) and propofol (5 mg mL-1) (ketofol). Each trachea was intubated and the rabbit administered oxygen during spontaneous ventilation. Ketofol infusion rate was initially 0.4 mg kg-1 minute-1 (0.2 mg kg-1 minute-1 of each drug) and was adjusted to maintain adequate anaesthetic depth based on clinical assessment. Ketofol dose and physiological variables were recorded every 5 minutes. Quality of sedation, intubation and recovery times were recorded. RESULTS: Ketofol induction doses decreased significantly in treatments AME (7.9 ± 2.3) and AMI (8.9 ± 4.0) compared with treatment Saline (16.8 ± 3.2 mg kg-1) (p < 0.05). The total ketofol dose to maintain anaesthesia was significantly lower in treatments AME, AMI and AMO (0.6 ± 0.1, 0.6 ± 0.2 and 0.6 ± 0.1 mg kg-1 minute-1, respectively) than in treatment Saline (1.2 ± 0.2 mg kg-1 minute-1) (p < 0.05). Cardiovascular variables remained at clinically acceptable values, but all treatments caused some degree of hypoventilation. CONCLUSIONS AND CLINICAL RELEVANCE: Premedication with AME, AMI and AMO, at the doses studied, significantly decreased the maintenance dose of ketofol infusion in rabbits. Ketofol was determined to be a clinically acceptable combination for TIVA in premedicated rabbits.

Clinical and Antinociceptive Effects of Distal Inferior Alveolar Nerve Block in Ponies With Tramadol 5% or Lidocaine 2.

This study aimed to compare the antinociceptive effects of tramadol 5% and lidocaine 2% on mental nerve block in horses of the Brazilian Pony breed. Eight adult non-pregnant mares were used in this study. The ponies were tranquilized with acepromazine (5 µg kg-1, IV), and the infiltration of the mental foramen was performed in Treatment 1- tramadol 5% (T, 150 mg) or Treatment 2- lidocaine 2% (L, 60 mg), both at a total dose of 3 ml in each foramen. Heart rate (HR), respiratory rate (RR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), rectal temperature (RT), and formation of skin lesions (SL) were evaluated. Evaluation of nociception of the outer lip (OL), inner lip (IL), and gingiva (GG) were performed using an electronic von Frey device with the evaluation of the ponies' reactions to each stimulus. From these reactions, we determined latency time (LT) and duration of antinociception (DAN). Analysis of variance with 16 observations was performed for HR, RR, SAP, DAP, MAP, LT and DAN. Data were expressed as mean ± standard deviation and the means were compared by the SNK and Student's t-test (P< 0.05). Changes in HR, RR, SAP, DAP, and MAP between evaluation times were associated with the effects of acepromazine (P>0.05). No formation of skin lesions was observed. Latency time did not differ between treatments (P>0.05). Both lidocaine 2% and tramadol 5% produced an antinociceptive effect. We conclude that the duration of the antinociceptive effect of tramadol 5% is longer than that of lidocaine 2%.

Comparison of the sedative effects of three nalbuphine doses, alone or combined with acepromazine, in dogs.

OBJECTIVE: To compare sedative, cardiopulmonary, and adverse effects of 3 nalbuphine doses, administered alone or in combination with acepromazine, in dogs. ANIMALS: 6 healthy dogs. PROCEDURES: Dogs were administered nalbuphine (1.0, 1.5, or 2.0 mg/kg, intravenously [IV]) combined with physiologic saline solution (1 mL, IV; treatments SN1.0, SN1.5, and SN2.0, respectively) or acepromazine (0.05 mg/kg, IV; treatments AN1.0, AN1.5, and AN2.0, respectively) in random order, with a 1-week washout interval between treatments. Sedation scores, heart rate, mean arterial pressure, respiratory rate, and rectal temperature were recorded before and 20 minutes after administration of saline solution or acepromazine (T0), and nalbuphine was administered at T0. Measurements were repeated 15, 30, 60, 90, and 120 minutes after nalbuphine administration. RESULTS: Treatments SN and AN resulted in at least 120 minutes of mild sedation and 60 minutes of moderate sedation, respectively. Sedation scores were greater for treatments AN1.0, AN1.5, and AN2.0 at various times, compared with scores for treatments SN1.0, SN1.5, and SN2.0, respectively. Administration of nalbuphine alone resulted in salivation and panting in some dogs. CLINICAL RELEVANCE: All nalbuphine doses promoted mild sedation when administered alone, and moderate sedation when combined with acepromazine. Greater doses of nalbuphine did not increase sedation scores. All treatments resulted in minimal changes in heart rate, respiratory rate, rectal temperature, and mean arterial pressure. Nalbuphine alone resulted in few adverse effects.

Sedative and cardiopulmonary effects of intramuscular combinations of hydromorphone, acepromazine, dexmedetomidine, and glycopyrrolate followed by intravenous propofol and inhalant isoflurane anesthesia in healthy dogs.

OBJECTIVE: To evaluate the sedative and cardiopulmonary effects of various combinations of acepromazine, dexmedetomidine, hydromorphone, and glycopyrrolate, followed by anesthetic induction with propofol and maintenance with isoflurane in healthy dogs. ANIMALS: 6 healthy adult female Beagles. PROCEDURES: Dogs were instrumented for hemodynamic measurements while anesthetized with isoflurane. Two hours after recovery, dogs received 1 of 4 IM combinations in a crossover design with 1 week between treatments: hydromorphone (0.1 mg/kg) and acepromazine (0.005 mg/kg; HA); hydromorphone and dexmedetomidine (0.0025 mg/kg; HD); hydromorphone, acepromazine, and dexmedetomidine (HAD); and hydromorphone, acepromazine, dexmedetomidine, and glycopyrrolate (0.02 mg/kg; HADG). Sedation was scored after 30 minutes. Physiologic variables and cardiac index were measured after sedation, after anesthetic induction with propofol, and every 15 minutes during maintenance of anesthesia with isoflurane for 60 minutes (target expired concentration at 760 mm Hg, 1.3%). RESULTS: Sedation scores were not significantly different among treatments. Mean ± SD cardiac index was significantly higher for the HA (202 ± 45 mL/min/kg) and HADG (185 ± 59 mL/min/kg) treatments than for the HD (88 ± 31 mL/min/kg) and HAD (103 ± 25 mL/min/kg) treatments after sedation and through the first 15 minutes of isoflurane anesthesia. No ventricular arrhythmias were noted with any treatment. CLINICAL RELEVANCE: In healthy dogs, IM administration of HADG before propofol and isoflurane anesthesia provided acceptable cardiopulmonary function with no adverse effects. This combination should be considered for routine anesthetic premedication in healthy dogs.

Effects of acepromazine and dexmedetomidine, followed by propofol induction and maintenance with isoflurane anaesthesia, on the microcirculation of Beagle dogs evaluated by sidestream dark field imaging: an experimental trial.

OBJECTIVE: To investigate the effects of intramuscularly administered acepromazine or dexmedetomidine on buccal mucosa microcirculation in Beagle dogs. STUDY DESIGN: Experimental, blinded, crossover study. ANIMALS: A group of seven Beagle dogs aged 7.5 ± 1.4 years (mean ± standard deviation). METHODS: Microcirculation was assessed on buccal mucosa using sidestream dark field videomicroscopy. After baseline measurements, 5 µg kg-1 dexmedetomidine or 30 µg kg-1 acepromazine were administered intramuscularly. After 10, 20 and 30 minutes, measurements were repeated. At 40 minutes after premedication, anaesthesia was induced with propofol intravenously and maintained with isoflurane. Measurements were repeated 50, 60 and 65 minutes after the injection of the investigated drugs. Analysed microcirculatory variables were: Perfused de Backer density, Perfused de Backer density of vessels < 20 µm, Proportion of perfused vessels and Proportion of perfused vessels < 20 µm. Heart rate (HR), systolic, diastolic (DAP) and mean (MAP) arterial pressures were recorded at the same time points. Macro- and microcirculatory variables were analysed using a linear mixed model with baseline as a covariate, treatment, trial period and repetition as fixed effects and time and dog as random effect. Results are presented as effect size and confidence interval; p values < 0.05 were considered significant. RESULTS: After acepromazine, Perfused de Backer density was greater during sedation and anaesthesia [3.71 (1.93-5.48 mm mm-2, p < 0.0001) and 2.3 (0.86-3.75 mm mm-2, p < 0.003)], respectively, than after dexmedetomidine. HR was significantly lower, whereas MAP and DAP were significantly higher with dexmedetomidine during sedation and anaesthesia (p < 0.0001 for all) compared with acepromazine. CONCLUSIONS AND CLINICAL RELEVANCE: The sedative drugs tested exerted a significant effect on buccal mucosal microcirculation with a higher Perfused de Backer density after the administration of acepromazine compared with dexmedetomidine. This should be considered when microcirculation is evaluated using these drugs.

A randomized clinical trial to compare ketamine-butorphanol-azaperone-medetomidine and detomidine-etorphine-acepromazine for anesthesia of captive Przewalski horses (Equus przewalskii).

OBJECTIVE: To compare ketamine-butorphanol-azaperone-medetomidine (KBAM) to detomidine-etorphine-acepromazine (DEA) for field anesthesia in captive Przewalski horses (Equus przewalskii). ANIMALS: 10 adult Przewalski horses. PROCEDURES: A prospective randomized crossover trial was conducted. Each horse was immobilized once with KBAM (200 mg ketamine, 109.2 mg butorphanol, 36.4 mg azaperone, and 43.6 mg medetomidine) and once with DEA (40 mg detomidine premedication, followed 20 minutes later by 3.9 to 4.4 mg etorphine and 16 to 18 mg acepromazine). Both protocols were administered by IM remote dart injection with a washout period of 6 months between treatments. Selected cardiorespiratory variables and quality of anesthesia were recorded. Antagonists were administered IM (KBAM, 215 mg atipamezole and 50 mg naltrexone; DEA, 4 mg RX821002 and 100 mg naltrexone). RESULTS: All horses were anesthetized and recovered uneventfully. Inductions (DEA, 6.8 min; KBAM, 11.6 min; P = 0.04) and recoveries (DEA, 3.2 min; KBAM, 19.6 min; P < 0.01) were faster with DEA compared with KBAM. Quality scores for induction and recovery did not differ between protocols, but maintenance quality was poorer for DEA (P < 0.01). Clinical concerns during DEA immobilizations included apnea, severe hypoxemia (arterial partial pressure of oxygen < 60 mm Hg), muscle rigidity, and tremors. Horses treated with KBAM were moderately hypoxemic, but arterial partial pressures of oxygen were higher compared with DEA (P < 0.01). CLINICAL RELEVANCE: Captive Przewalski horses are effectively immobilized with KBAM, and this protocol results in superior muscle relaxation and less marked hypoxemia during the maintenance phase, but slower inductions and recoveries, compared with DEA.

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

OBJECTIVE: To determine the effects of intravenous (IV) premedication with acepromazine, butorphanol or their combination, on the propofol anesthetic induction dosage in dogs. STUDY DESIGN: Prospective, blinded, Latin square design. ANIMALS: A 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. METHODS: Each 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). RESULTS: Propofol 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 RELEVANCE: Although the largest decrease in propofol dosage required for intubation was after IV premedication with acepromazine and butorphanol, hypotension and apnea still occurred.

Immobilization of captive plains zebras (Equus quagga) with a combination of etorphine hydrochloride, acepromazine, and xylazine hydrochloride.

The plains zebra (Equus quagga) is a zebra species commonly kept in zoos around the world. However, they are not tame like their domestic relatives and are difficult to immobilize. We immobilized 30 captive plains zebra with a combination of etorphine hydrochloride (2-4 mg), acepromazine (8 mg), and xylazine hydrochloride (30 or 50 mg) to perform physical examination and blood sample collection for disease diagnostics. Physiological parameters including heart rate, respiratory rate, body temperature, and hemoglobin oxygen saturation were recorded. All zebras exhibited satisfactory anesthesia and fully recovered without re-narcotization. The results suggest that etorphine hydrochloride-acepromazine-xylazine hydrochloride combination for plains zebra immobilization is a safe and sufficient regimen for short procedures such as wellness examinations and sample collection.

Effectiveness of orally administered maropitant and ondansetron in preventing preoperative emesis and nausea in healthy dogs premedicated with a combination of hydromorphone, acepromazine, and glycopyrrolate.

OBJECTIVE: To compare effectiveness of maropitant and ondansetron in preventing preoperative vomiting and nausea in healthy dogs premedicated with a combination of hydromorphone, acepromazine, and glycopyrrolate. ANIMALS: 88 dogs owned by rescue organizations. PROCEDURES: Dogs received maropitant (n = 29) or ondansetron (28) PO 2 hours prior to premedication or did not receive an antiemetic (31; control). Dogs were evaluated for vomiting, nausea, and severity of nausea (scored for 6 signs) for 15 minutes following premedication with hydromorphone, acepromazine, and glycopyrrolate. RESULTS: A significantly lower percentage of dogs vomited after receiving maropitant (3/29 [10%]), compared with control dogs (19/31 [62%]) and dogs that received ondansetron (15/28 [54%]). A significantly lower percentage of dogs appeared nauseated after receiving maropitant (3/29 [10%]), compared with control dogs (27/31 [87%]) and dogs that received ondansetron (14/28 [50%]), and a significantly lower percentage of dogs appeared nauseated after receiving ondansetron, compared with control dogs. Nausea severity scores for hypersalivation, lip licking, hard swallowing, and hunched posture were significantly lower for dogs that received maropitant than for control dogs, and scores for hypersalivation, lip licking, and hard swallowing were significantly lower for dogs that received ondansetron than for control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Oral administration of maropitant 2 hours prior to premedication with hydromorphone reduced the incidence of vomiting and the incidence and severity of nausea in healthy dogs. Oral administration of ondansetron reduced the incidence and severity of nausea but not the incidence of vomiting.

Conventional and advanced echocardiographic assessment of systolic function in dogs sedated with dexmedetomidine or acepromazine.

Dexmedetomidine and acepromazine, sedatives commonly used in dogs have opposite vascular effects, resulting in afterload increase and decrease, respectively. This could variably affect systolic myocardial function. Previous echocardiographic studies assessing the cardiovascular effects of these drugs used conventional echocardiography, while advanced techniques such as speckle tracking echocardiography (STE) and tissue Doppler imaging (TDI), which are known to provide a more accurate assessment of systolic function, have been rarely used for this aim. Moreover, in the few studies using advanced techniques, the drugs where combined with opioids. Therefore, the main objective of this prospective study was to assess systolic myocardial function by conventional and advanced echocardiography (STE and TDI), in dogs sedated exclusively with dexmedetomidine or acepromazine not combined with other drugs. Twenty healthy dogs were randomly divided into two groups, Group A (acepromazine, 20 µg/kg IM), and Group D (dexmedetomidine, 5 µg/kg IM), cardiovascular parameters were assessed before sedation (T0), and thirty minutes afterwards (T1). Systolic arterial pressure and heart rate decreased in both groups at T1 as compared to T0. Only one conventional echocardiographic raw variable (left ventricular internal dimension in systole) and three out of five advanced echocardiographic variables (radial TDI systolic velocities at the epicardial region of the left ventricular free wall, longitudinal TDI systolic velocities of the septal mitral valve annulus and the STE-derived left ventricular global strain), were affected in Group D. A systolic impairment was observed in Group D and better estimated by advanced echocardiography. In Group A, only the end diastolic voume index (conventional echocardiography) was decreased. Both protocols seem to induce echocardiographic changes more likely secondary to their vascular action.

Evaluation of whether acepromazine maleate causes fentanyl to decrease the minimum alveolar concentration of isoflurane in cats.

OBJECTIVE: To determine whether isoflurane-anesthetized cats with demonstrated resistance to the immobilizing effects of fentanyl would exhibit naltrexone-reversible sparing of the minimum alveolar concentration (MAC) of isoflurane when fentanyl was coadministered with the centrally acting catecholamine receptor antagonist acepromazine. ANIMALS: 5 healthy male purpose-bred cats. PROCEDURES: Anesthesia was induced and maintained with isoflurane in oxygen. Baseline isoflurane MAC was measured by use of a standard tail clamp stimulus and bracketing study design. Afterward, fentanyl was administered IV to achieve a plasma concentration of 100 ng/mL by means of target-controlled infusion, and isoflurane MAC was remeasured. Next, acepromazine maleate (0.1 mg/kg) was administered IV, and isoflurane MAC was remeasured. Finally, isoflurane concentration was equilibrated at 70% of the baseline MAC. Movement of cats in response to tail clamping was tested before and after IV bolus administration of naltrexone. Physiologic responses were compared among treatment conditions. RESULTS: Isoflurane MAC did not differ significantly between baseline and fentanyl infusion (mean ± SD, 1.944 ± 0.111% and 1.982 ± 0.126%, respectively). Acepromazine with fentanyl significantly decreased isoflurane MAC to 1.002 ± 0.056% of 1 atm pressure. When isoflurane was increased to 70% of the baseline MAC, no cats moved in response to tail clamping before naltrexone administration, but all cats moved after naltrexone administration. CONCLUSIONS AND CLINICAL RELEVANCE: Acepromazine caused fentanyl to decrease the isoflurane MAC in cats that otherwise did not exhibit altered isoflurane requirements with fentanyl alone. Results suggested that opioid-mediated increases in brain catecholamine concentrations in cats counteract the opioid MAC-sparing effect.

Cardiopulmonary effects of an intravenous infusion of fentanyl in cats during isoflurane anesthesia and with concurrent acepromazine or dexmedetomidine administration during anesthetic recovery.

OBJECTIVE: To determine the cardiopulmonary effects of IV administration of fentanyl to cats anesthetized with isoflurane and during anesthetic recovery with concurrent administration of acepromazine or dexmedetomidine. ANIMALS: 6 healthy adult cats. PROCEDURES: Cats received an IV bolus (5 µg/kg) followed by an IV infusion (5 µg/kg/h) of fentanyl for 120 minutes during isoflurane anesthesia and for 30 minutes after discontinuing isoflurane. Cats were randomly assigned in a crossover study to receive acepromazine (0.05 mg/kg) or dexmedetomidine (2.5 µg/kg), IV, when isoflurane was discontinued. Cardiopulmonary data were obtained during anesthesia and for 30 minutes during the anesthetic recovery period. RESULTS: The administration of fentanyl during isoflurane anesthesia resulted in a transient increase in arterial blood pressure, mean pulmonary artery pressure, and oxygen delivery. Compared with values during isoflurane anesthesia, administration of dexmedetomidine during anesthetic recovery resulted in significant decreases in cardiac index, stroke index, and oxygen delivery and significant increases in arterial, central venous, and mean pulmonary artery pressures; systemic vascular resistance index; and oxygen extraction ratio. Administration of acepromazine resulted in increases in heart rate, cardiac index, oxygen uptake, and oxygen extraction ratio. Oxygen extraction ratio did not differ between acepromazine and dexmedetomidine. CONCLUSIONS AND CLINICAL RELEVANCE: Fentanyl transiently improved indices of cardiopulmonary performance when administered to healthy cats anesthetized with isoflurane. The cardiovascular effects of acepromazine and dexmedetomidine in healthy cats receiving fentanyl during recovery from isoflurane anesthesia differed, but measured cardiopulmonary parameters remained within acceptable limits.

Dose requirement and cardiopulmonary effects of diluted and undiluted propofol for induction of anaesthesia in dogs.

OBJECTIVE: To compare the dose, cardiopulmonary effects and quality of anaesthetic induction in dogs using propofol (10 mg mL-1) and diluted propofol (5 mg mL-1). STUDY DESIGN: Randomized, blinded, clinical study. ANIMALS: A total of 28 client-owned dogs (12 males/16 females). METHODS: Following intramuscular acepromazine (0.02 mg kg-1) and methadone (0.2 mg kg-1), propofol (UP, 10 mg mL-1) or diluted propofol (DP, 5 mg mL-1) was administered intravenously (0.2 mL kg-1 minute-1) by an anaesthetist unaware of the allocated group to achieve tracheal intubation. Sedation, intubation and induction quality were scored from 0 to 3. Pre- and post-induction pulse rate (PR), respiratory rate (fR) and systolic (SAP), mean (MAP) and diastolic (DAP) arterial blood pressure were compared. Time to first breath and induction dose were recorded. Data were analysed for normality and Mann-Whitney U or Student t tests were performed where appropriate. Significance was set at p < 0.05. Data are presented as mean ± standard deviation or median (range). RESULTS: The propofol dose administered to achieve induction was lower in the DP group (2.62 ± 0.48 mg kg-1) than in the UP group (3.48 ± 1.17 mg kg-1) (p = 0.021). No difference was observed in pre- and post-induction PR, SAP, MAP, DAP and fR between groups. The differences between post-induction and pre-induction values of these variables were also similar between groups. Time to first breath did not differ between groups. Sedation scores were similar between groups. Quality of tracheal intubation was marginally better with UP 0 (0-1) than with DP 1 (0-2) (p = 0.036), but overall quality of induction was similar between groups [UP 0 (0-1) and DP 0 (0-1), p = 0.549]. CONCLUSION AND CLINICAL RELEVANCE: Diluting propofol reduced the dose to induce anaesthesia without significantly altering the cardiopulmonary variables.

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.

Comparison of the effects of methadone and butorphanol combined with acepromazine for canine gastroduodenoscopy.

OBJECTIVE: To evaluate the feasibility of gastroduodenoscopy in dogs premedicated with acepromazine in combination with butorphanol or methadone. STUDY DESIGN: Prospective, randomized, double-blinded clinical trial. ANIMALS: A group of 40 client-owned dogs. METHODS: Dogs were randomly allocated to one of two groups and give intramuscular acepromazine 0.02 mg kg-1 combined with either butorphanol 0.3 mg kg-1 (group ACEBUT) or methadone 0.2 mg kg-1 (group ACEMET). General anaesthesia was induced with propofol and ketamine and maintained with sevoflurane (2.3%) in oxygen. Cardiopulmonary variables were recorded at 5 minute intervals during anaesthesia. Feasibility of the entire gastroduodenoscopy was evaluated with a visual analogue scale (VAS) from 0 (best) to 100 (worst) (primary outcome of the study). Lower oesophageal sphincter dilatation and duodenal intubation were scored. Pylorus diameter was measured with standard endoscopic inflatable balloons. Overall cardiovascular stability was assessed during anaesthesia, using a VAS (0-100), as was the presence of fluid in the oesophagus, regurgitation, need for mechanical ventilation, and intraoperative and postoperative rescue analgesia (secondary outcomes of the study). Differences between treatments were analysed with Mann-Whitney U, Student t test, Fisher exact test or mixed model analysis of variance as appropriate. Subsequently, feasibility VAS of the gastroduodenoscopy was assessed for noninferiority between groups. The noninferiority margin was set as -10. RESULTS: All gastroduodenoscopies were successfully completed in both groups using an endoscope tip diameter of 12.8 mm in all but one dog. Feasibility of gastroduodenoscopy was evaluated as 2.9 ± 5.6 in group ACEBUT and 5.1 ± 5.8 in group ACEMET. No significant differences between groups were detected in any measured or assessed variables, and noninferiority was confirmed. CONCLUSION AND CLINICAL RELEVANCE: In our study population, the effects of methadone and butorphanol when combined with acepromazine were comparable.