Use of midlatency auditory-evoked potentials as indicator of unconsciousness in the dog: characterisation of the effects of acepromazine-thiopentone, medetomidine-thiopentone and medetomidine-butorphanol-midazolam combinations.

Middle latency auditory-evoked potentials were measured in sedated and anaestetised dogs to determine their possible usefulness in monitoring of unconsciousness during anaesthesia and to compare the effects of anaesthetic protocols. There were three groups of five dogs: group I received acepromazine; groups 2 and 3 received medetomidine; 30 minutes later, groups 1 and 2 received thiopentone and group 3 received midazolam and butorphanol. Groups 2 and 3 received atipamezole 60 minutes after medetomidine was administered. Auditory-evoked potentials were recorded at time 15, 40 and 75 minutes. Thiopentone administration resulted in a profound modification of the pattern of response, and several peaks were no longer identified. In group 3, the administration of midazolam-butorphanol tended to increase the latency of the different peaks, but lesser than thiopentone did. Middle latency-evoked potentials appeared to be potentially useful in the monitoring of unconsciousness in the dog.     

Seizures during medetomindine sedation and local anaesthesia in two dogs undergoing skin biopsy

Each of two dogs presented for multiple skin biopsies were sedated with intravenous medetomidine and lignocaine was injected subcutaneously to provide local anaesthesia for skin biopsy. One dog had a seizure during skin biopsy and again immediately following reversal of medetomidine with atipamezole. The other dog developed seizures 2 h following skin biopsy at which time the medetomidine was reversed with atipamezole. Both dogs were neurologically normal with no history of seizures prior to the procedure and remained neurologically normal for 14 weeks and 9 months, respectively, following the procedure. A drug interaction between the α₂-adrenergic agonist medetomidine and lignocaine is suspected and highlights the potential for seizures following the subcutaneous administration of relatively large doses of lignocaine under medetomidine sedation.     

Cerebral state monitoring in Beagle dogs sedated with medetomidine

OBJECTIVE: To provide experience of monitoring the level of hypnosis with the Cerebral State Monitor (CSM), a device extracting a single numerical variable between 0 and 100 from the electroencephalogram in dogs sedated with medetomidine during dental scale removal. STUDY DESIGN: Prospective observational study. Animals Nine female Beagle dogs weighing 13.3 +/- 1.3 kg. METHODS: Cerebral state index (CSI) and burst suppression ratio (BSR) were recorded from sub-dermal needle electrodes in dogs sedated after subcutaneous injection of 114 +/- 11 microg kg(-1) medetomidine. Ten minutes after injection CSI monitoring began, and after 5 minutes, dental scale removal with an ultrasonic probe was started. After approximately 30 minutes, the effects of medetomidine were antagonized with atipamezole. RESULTS: The CSI had a median value of 43 (range 40-56) in undisturbed sedated dogs. During dental scale removal, CSI increased to a median value of 99 (range 92-100). The BSR in undisturbed sedated dogs ranged from 2 to 15, but fell to zero during dental scale removal. CONCLUSIONS: Stimulation during dental scale removal might be expected to reduce the level of sedation and hypnosis in dogs to which medetomidine had been administered. The concurrent increase in CSI and decrease in BSR suggested that a higher CSI was associated with arousal from sedation and a reduction in the depth of hypnosis. More studies are needed to validate CSI in order to better understand the functioning of this monitor. CLINICAL RELEVANCE: The CSM shows promise for monitoring the degree of sedation and hypnosis during anaesthesia, and after adequate validation, could contribute to the refinement of anaesthetic techniques in animals.     

A comparison of the sedative and analgesic effects of buprenorphine in combination with acepromazine, midazolam or medetomidine in dogs

The effects of buprenorphine in combination with acepromazine, midazolam or medetomidine were compared in dogs. Induction and recovery times, heart rate, respiratory rate and body temperature were measured. Posture, reaction to noise, analgesia and muscle relaxation were assessed and a global score of "sedation-analgesia" was calculated. There were 3 groups of 4 animals: group 1 received 0.1 mg.kg-¹ acepromazine IM and 20 minutes later, 10 g.kg-¹ buprenorphine IV; group 2 received 1 mg.kg-¹ midazolam IV simultaneously with 10 ig.kg-¹ buprenorphine IV and group 3 received 1 mg/m² body surface area medetomidine IM and 20 minutes later, 10 Hg.kg-¹ buprenorphine IV. Only one dog given acepromazine and buprenorphine reached a "sedation-analgesia" stage, denned as the inability to stand together with the absence of reaction to stimulation, including pain. Animals in this group showed a decrease in respiratory rate and in body temperature. None of the dogs given midazolam and buprenorphine became sedated or showed signs of analgesia. Following this combination, the dogs were excited and showed dysphoric reactions which disappeared within 20 minutes.
All of the dogs given medetomidine and buprenorphine showed good sedation and analgesia lasting more than 20 minutes. This drug combination produced a decrease in heart and respiratory rates and body temperature.     

Effects of medetomidine,l‐methadone,and their combination on arterial blood gases in dogs

ObjectiveTo investigate the influence of l–methadone on medetomidine–induced changes in arterial blood gases and clinical sedation in dogs.Study designProspective experimental cross–over study (Latin square design).AnimalsFive 1–year–old purpose bred laboratory beagle dogs of both sexes.MethodsEach dog was treated three times: medetomidine (20 μg kg^?1 IV), l–methadone (0.1 mg kg^?1 IV) and their combination. Arterial blood was collected for blood gas analysis. Heart and respiratory rates were recorded, and clinical sedation and reaction to a painful stimulus were scored before drug administration and at various time points for 30 minutes thereafter.ResultsArterial partial pressure of oxygen decreased slightly after medetomidine administration and further after medetomidine/l–methadone administration (range 55.2–86.7 mmHg, 7.4–11.6 kPa, at 5 minutes). A slight increase was detected in arterial partial pressure of carbon dioxide after administration of l–methadone and medetomidine/l–methadone (42.6 ± 2.9 and 44.7 ± 2.4 mmHg, 5.7 ± 0.4 and 6.0 ± 0.3 kPa, 30 minutes after drug administration, respectively). Arterial pH decreased slightly after administration of l–methadone and medetomidine/l–methadone. Heart and respiratory rates decreased after administration of medetomidine and medetomidine/l–methadone, and no differences were detected between the two treatments. Most dogs panted after administration of l–methadone and there was slight sedation. Medetomidine induced moderate or deep sedation, and all dogs were deeply sedated after administration of medetomidine/l–methadone. Reaction to a noxious stimulus was strong or moderate after administration of methadone, moderate or absent after administration of medetomidine, and absent after administration of medetomidine/l–methadone.Conclusions and clinical relevanceAt the doses used in this study, l–methadone potentiated the sedative and analgesic effects and the decrease in arterial oxygenation induced by medetomidine in dogs, which limits the clinical use of this combination.     

Evaluation of some drug combinations for sedation in the dog

A double blind trial was performed in order to investigate the effects of some sedatives in the dog. One hundred and forty-two dogs undergoing radiography for the BVA/KC hip dysplasia scheme were sedated with combinations of acepromazine with pethidine or buprenorphine, or with acepromazine alone. The degree of sedation, resistance to manipulation, sensitivity to noise and response to pain were assessed, and arterial blood samples taken for blood gas analysis. In all respects the combinations of acepromazine with buprenorphine or pethidine produced significantly better sedation than acepromazine alone. Pa0₂ and pH were lower and PaCO₂ higher in dogs receiving the combinations compared with those receiving acepromazine alone, but all values were within normal limits. It was concluded that combinations of pethidine or buprenorphine with acpromazine provide extremely effective and safe sedation in the dog.     

Evaluation of the perioperative stress response in dogs administered medetomidine or acepromazine as part of the preanesthetic medication

OBJECTIVE: To compare the perioperative stress response in dogs administered medetomidine or acepromazine as part of the preanesthetic medication. ANIMALS: 42 client-owned dogs that underwent elective ovariohysterectomy. PROCEDURE: Each dog was randomly allocated to receive medetomidine and butorphanol tartrate (20 microgram/kg and 0.2 mg/kg, respectively, IM) or acepromazine maleate and butorphanol (0.05 and 0.2 mg/kg, respectively, IM) for preanesthetic medication. Approximately 80 minutes later, anesthesia was induced by administration of propofol and maintained by use of isoflurane in oxygen. Each dog was also given carprofen before surgery and buprenorphine after surgery. Plasma concentrations of epinephrine, norepinephrine, cortisol, and beta-endorphin were measured at various stages during the perioperative period. In addition, cardiovascular and clinical variables were monitored. RESULTS: Concentrations of epinephrine, norepinephrine, and cortisol were significantly lower for dogs administered medetomidine. Concentrations of beta-endorphin did not differ between the 2 groups. Heart rate was significantly lower and mean arterial blood pressure significantly higher in dogs administered medetomidine, compared with values for dogs administered acepromazine. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that for preanesthetic medications, medetomidine may offer some advantages over acepromazine with respect to the ability to decrease perioperative concentrations of stress-related hormones. In particular, the ability to provide stable plasma catecholamine concentrations may help to attenuate perioperative activation of the sympathetic nervous system.     

Cardiorespiratory effects of desflurane in dogs given romifidine or medetomidine before induction of anesthesia with propofol

The objective of this study was to evaluate the use of desflurane after induction of anesthesia with propofol in dogs sedated with romifidine or medetomidine. Each of 8 healthy dogs received intravenously, in random order, 3 preanesthetic protocols: romifidine, 40 microg/kg of body weight (BW) (R40); romifidine, 80 microg/kg BW (R80); and medetomidine, 10 microg/kg BW (MED). Cardiovascular and respiratory variables were recorded during the procedure. Time to extubation, time to sternal recumbency, and time to standing were also recorded. Heart rate and respiratory rate decreased significantly during sedation from baseline values, but there were no differences between the means for the 3 preanesthetic protocols. Mean values for heart rate, mean arterial blood pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation, end-tidal CO2 level, pH, and arterial blood gas values during anesthesia were similar for the 3 protocols. The mean end-tidal desflurane concentration was significantly lower with the R80 protocol than with the R40 protocol. The mean time to extubation was significantly shorter with the R40 protocol than with the R80 and MED protocols.     

Reversal of medetomidine sedation by atipamezole in dogs

Atipamezole reversed the sedative effect of medetomidine in twelve laboratory beagles. The dogs were sedated with medetomidine doses of 20, 40 and 80 micrograms/kg body wt i.m. Atipamezole was injected (i.m.) 20 min later at dose rates two, four, six and ten times higher (in micrograms/kg) than the preceding medetomidine dose. Placebo treatment was included in the study. The deeply sedated dogs showed signs of arousal in 3-7 min and took their first steps 4-12 min after atipamezole injection. The dose-related reversal effect of atipamezole proved to be optimal with doses which were four, six or ten times higher than the preceding medetomidine dose. Drowsiness was found 0.5-1 h after atipamezole injection in 41% of the cases. No adverse effects nor cases of over-alertness or excitement were found.     

Effects of acepromazine on the incidence of vomiting associated with opioid administration in dogs

Objective To evaluate the anti‐emetic properties of acepromazine in dogs receiving opioids as pre‐anesthetic medication. Study design Randomized prospective clinical study. Animals One hundred and sixteen dogs (ASA I or II), admitted for elective surgical procedures. The dogs were a mixed population of males and females, purebreds and mixed breeds, 0.25–13.4 years of age, weighing 1.8–57.7 kg. Methods A prospective clinical trial in which the dogs were randomly assigned to one of three groups. All groups received acepromazine (0.05 mg kg^?1 intramuscularly (IM)). Group I received acepromazine 15 minutes prior to opioid administration. Group II received acepromazine in combination with the opioid. Group III received acepromazine 15 minutes after opioid administration. One of three different opioids was administered IM to each dog: morphine sulfate at 0.5 mg kg^?1; hydromorphone hydrochloride at 0.1 mg kg^?1; or oxymorphone hydrochloride at 0.075 mg kg^?1. Results Dogs receiving acepromazine before the opioid (group I) had a significantly lower incidence of vomiting (18%) than dogs in groups II (45%) and III (55%). The degree of sedation was significantly lower in the dogs receiving the combination of acepromazine and the opioid (group II) than in dogs receiving the opioid as the first drug (group III). Conclusions and clinical relevance Acepromazine administered 15 minutes before the opioid lowers the incidence of vomiting induced by opioids.     

Sedative and cardiopulmonary effects of medetomidine hydrochloride and xylazine hydrochloride and their reversal with atipamezole hydrochloride in calves

OBJECTIVE: To assess the sedative and cardiopulmonary effects of medetomidine and xylazine and their reversal with atipamezole in calves. ANIMALS: 25 calves. PROCEDURES: A 2-phase (7-day interval) study was performed. Sedative characteristics (phase I) and cardiopulmonary effects (phase II) of medetomidine hydrochloride and xylazine hydrochloride administration followed by atipamezole hydrochloride administration were evaluated. In both phases, calves were randomly allocated to receive 1 of 4 treatments IV: medetomidine (0.03 mg/kg) followed by atipamezole (0.1 mg/kg; n = 6), xylazine (0.3 mg/kg) followed by atipamezole (0.04 mg/kg; 7), medetomidine (0.03 mg/kg) followed by saline (0.9% NaCl; 6) solution (10 mL), and xylazine (0.3 mg/kg) followed by saline solution (10 mL; 6). Atipamezole or saline solution was administered 20 minutes after the first injection. Cardiopulmonary variables were recorded at intervals for 35 minutes after medetomidine or xylazine administration. RESULTS: At the doses evaluated, xylazine and medetomidine induced a similar degree of sedation in calves; however, the duration of medetomidine-associated sedation was longer. Compared with pretreatment values, heart rate, cardiac index, and PaO(2) decreased, whereas central venous pressure, PaCO(2), and pulmonary artery pressures increased with medetomidine or xylazine. Systemic arterial blood pressures and vascular resistance increased with medetomidine and decreased with xylazine. Atipamezole reversed the sedative and most of the cardiopulmonary effects of both drugs. CONCLUSIONS AND CLINICAL RELEVANCE: At these doses, xylazine and medetomidine induced similar degrees of sedation and cardiopulmonary depression in calves, although medetomidine administration resulted in increases in systemic arterial blood pressures. Atipamezole effectively reversed medetomidine- and xylazine-associated sedative and cardiopulmonary effects in calves.     

The clinical effectiveness of atipamezole as a medetomidine antagonist in the dog

The efficacy of atipamezole, a recently introduced alpha 2-adrenoceptor antagonist, in reversing medetomidine-induced effects in dogs was investigated in a clinical study. Dogs from eight Finnish small-animal hospitals were sedated with a 40-microgram/kg dose of the alpha 2-agonist medetomidine i.m. In the first part of the study (n = 319), a randomized, double-blind design with respect to the dose of atipamezole (0, 80, 160 and 240 micrograms/kg i.m.) was used. In a separate study (n = 358), which was an open trial, the selected dose of atipamezole was 200 micrograms/kg i.m. Atipamezole at dose rates of 80-240 micrograms/kg rapidly and effectively reversed medetomidine-induced deep sedation-analgesia, recumbency and bradycardia. The median arousal time after atipamezole was 3-5 min, and walking time was 6-10 min compared to greater than 30 min for both effects after placebo. Heart rate also increased in a dose-related manner after atipamezole administration. The investigators' overall evaluation of the ability of atipamezole to reverse the effects of medetomidine was 'good' in 90%, and 'moderate' in 9% of cases. Relapse into sedation was reported in three individual cases. Side-effects were minimal. It is concluded that at doses four- to sixfold the medetomidine dose, atipamezole is a highly effective and safe agent in reversing medetomidine-induced sedation-analgesia, recumbency and bradycardia in dogs in veterinary practice.     

Feline pyothorax - new insights into an old problem: part 1. Aetiopathogenesis and diagnostic investigation

Relationships between onset latency and peak-to-peak amplitude of magnetic motor evoked potentials (MMEP) after transcranial magnetic stimulation (TMS), together with the electroencephalographic parameters bispectral analysis index (BIS) and the autoregressive model with exogenous input (ARX)-derived auditory evoked potential index (AAI) were explored during different sedative and hypnotic drug combinations in six dogs. TMS was performed under sedation with acepromazine/methadone or medetomidine and after a single bolus injection of propofol or etomidate. Data for BIS and AAI were continuously collected during the periods of treatment with the hypnotic drugs. Changes in BIS and AAI during both periods were not statistically correlated with changes in onset latencies and peak-to-peak amplitudes of MMEP after TMS. Therefore, both electroencephalographic techniques are of limited use in titrating sedation and anaesthesia during TMS in the dog.     

Chemical restraint by medetomidine and medetomidine–midazolam and its reversal by atipamezole in Japanese macaques (Macaca fuscata)

Objective To evaluate the sedative effects of medetomidine, and a medetomidine–midazolam combination, in Japanese macaques and the antagonism of medetomidine–midazolam with atipamezole. Study design Prospective randomized study. Animals Thirteen healthy Japanese macaques between 3 and 21 years old and weighing between 4.3 and 15.1 kg. Methods Medetomidine (120 µg kg^?1) alone or a medetomidine (30 µg kg^?1) plus midazolam (0.3 mg kg^?1) mixture were injected intramuscularly in the hind limb of 12 animals (n = 6 for each group) and their effects, particularly behavioural changes, response to external stimuli, sedative onset time, time to lateral recumbency and time in lateral recumbency, were monitored for 120 minutes. Another group (n = 7) were given medetomidine–midazolam and injected 30 minutes later with atipamezole (120 µg kg^?1). Behavioural changes and responses to external stimuli were assessed as before. Results Animals given medetomidine became sedated but could be aroused by external stimuli. Despite the lower (25%) dose of medetomidine involved, the effects of medetomidine–midazolam were more marked. Macaques given this combination became sedated in 4 ± 2 minutes (mean ± SD) and remained unresponsive to external stimuli for at least 60 minutes. Five out of six macaques became laterally recumbent for 74 ± 37 minutes. Intramuscular atipamezole effectively reversed sedation, shortening the arousal and total recovery time. The recovery from sedation was rapid and smooth, being completed 19 ± 11 minutes after antagonism. Conclusions The medetomidine–midazolam combination described provided useful chemical restraint and may prove useful in macaques undergoing some experimental, diagnostic or therapeutic procedures. The use of atipamezole as an antagonist increases the value of this technique in macaques.     

Effects of methadone, alone or in combination with acepromazine or xylazine, on sedation and physiologic values in dogs

ObjectiveTo evaluate the effects of methadone, administered alone or in combination with acepromazine or xylazine, on sedation and on physiologic values in dogs.Study designRandomized cross-over design.AnimalsSix adult healthy mixed-breed dogs weighing 13.5 ± 4.9 kg.MethodsDogs were injected intramuscularly with physiologic saline (Control), or methadone (0.5mg kg⁻¹) or acepromazine (0.1 mg kg⁻¹) or xylazine (1.0 mg kg⁻¹), or acepromazine (0.05 mg kg⁻¹) plus methadone (0.5 mg kg⁻¹) or xylazine (0.5 mg kg⁻¹) plus methadone (0.5 mg kg⁻¹) in a randomized cross-over design, with at least 1-week intervals. Sedation, pulse rate, indirect systolic arterial pressure, respiratory rate (RR), body temperature and pedal withdrawal reflex were evaluated before and at 15-minute intervals for 90 minutes after treatment.ResultsSedation was greater in dogs receiving xylazine alone, xylazine plus methadone and acepromazine plus methadone. Peak sedative effect occurred within 30 minutes of treatment administration. Pulse rate was lower in dogs that received xylazine either alone or with methadone during most of the study. Systolic arterial pressure decreased only in dogs receiving acepromazine alone. When methadone was administered alone, RR was higher than in other treatments during most of the study and a high prevalence of panting was observed. In all treatments body temperature decreased, this effect being more pronounced in dogs receiving methadone alone or in combination with acepromazine. Pedal withdrawal reflex was absent in four dogs receiving methadone plus xylazine but not in any dog in the remaining treatments.Conclusions and clinical relevanceMethadone alone produces mild sedation and a high prevalence of panting. Greater sedation was achieved when methadone was used in combination with acepromazine or xylazine. The combination xylazine–methadone appears to result in better analgesia than xylazine administered alone. Both combinations of methadone/sedative were considered effective for premedication in dogs.     

Effects of medetomidine and medetomidine-butorphanol combination on Schirmer tear test 1 readings in dogs

Medetomidine is a commonly used sedative in veterinary medicine whether administered alone or in combination with an opioid such as butorphanol. There are no previous studies that look at the effects of this drug on sequential Schirmer tear test (STT) 1 readings in dogs, including effects on tear production after reversal of the drug. The present study looked at two groups of 10 dogs each that were sedated with intravenous medetomidine or a combination of medetomidine and butorphanol. All dogs had tear readings taken presedation, 15 min postsedation, and 15 min after reversal of medetomidine with atipamezole. Results revealed that intravenous sedation with medetomidine and medetomidine-butorphanol in dogs with no history of ophthalmic disease and presedation STT 1 readings above 15 mm/min, causes a significant decrease in tear production that is measurable at 15 min postsedation. Readings returned to near presedation values within 15 min postreversal in most cases. It is therefore recommended that all eyes be treated with a tear substitute from the time the sedative is given until at least 15 min after reversal.     

Sedative and cardiorespiratory effects of medetomidine, medetomidine-butorphanol, and medetomidine-ketamine in dogs

OBJECTIVE: To determine sedative and cardiorespiratory effects of i.m. administration of medetomidine alone and in combination with butorphanol or ketamine in dogs. DESIGN: Randomized, crossover study. ANIMALS: 6 healthy adult dogs. PROCEDURES: Dogs were given medetomidine alone (30 micrograms/kg [13.6 micrograms/lb] of body weight, i.m.), a combination of medetomidine (30 micrograms/kg, i.m.) and butorphanol (0.2 mg/kg [0.09 mg/lb], i.m.), or a combination of medetomidine (30 micrograms/kg, i.m.) and ketamine (3 mg/kg [1.36 mg/lb], i.m.). Treatments were administered in random order with a minimum of 1 week between treatments. Glycopyrrolate was given at the same time. Atipamezole (150 micrograms/kg [68 micrograms/lb], i.m.) was given 40 minutes after administration of medetomidine. RESULTS: All but 1 dog (given medetomidine alone) assumed lateral recumbency within 6 minutes after drug administration. Endotracheal intubation was significantly more difficult when dogs were given medetomidine alone than when given medetomidine and butorphanol. At all evaluation times, percentages of dogs with positive responses to tail clamping or to needle pricks in the cervical region, shoulder region, abdominal region, or hindquarters were not significantly different among drug treatments. The Paco2 was significantly higher and the arterial pH and Pao2 were significantly lower when dogs were given medetomidine and butorphanol or medetomidine and ketamine than when they were given medetomidine alone. Recovery quality following atipamezole administration was unsatisfactory in 1 dog when given medetomidine and ketamine. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that a combination of medetomidine with butorphanol or ketamine resulted in more reliable and uniform sedation in dogs than did medetomidine alone.     

Effect of medetomidine infusion on the anaesthetic requirements of desflurane in dogs

The objective of this paper was to evaluate the effect of constant rate infusion of medetomidine on the anaesthetic requirements of desflurane in dogs. For this, six healthy dogs were studied. Measurements for baseline were taken in the awake, unsedated dogs, then each dog received intravenously (i.v.) three anaesthetic protocols: M (no medetomidine infusion), M0.5 (infusion of medetomidine at 0.5 microg/kg/h, i.v.) or M1 (infusion of medetomidine at 1 microg/kg/h, i.v.). All dogs were sedated with medetomidine (2 microg/kg, i.v.) and measurements repeated in 10 min. Induction of anaesthesia was delivered with propofol (3 mg/kg, i.v.) and maintained with desflurane for 90 min to achieve a defined surgical plane of anaesthesia in all cases. After tracheal intubation infusion of medetomidine was initiated and maintained until the end of anaesthesia. Cardiovascular, respiratory, arterial pH (pHa) and arterial blood gas tensions (PaO(2), PaCO(2)) variables were measured during the procedure. End tidal desflurane concentration (EtDES) was recorded throughout anaesthesia. Time to extubation, time to sternal recumbency and time to standing were also noted. Heart rate and respiratory rate were significantly decreased during sedation in all protocols compared to baseline values. Mean heart rate, mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation, end-tidal CO(2), pHa, PaO(2), and PaCO(2) during anaesthesia were similar for all protocols. EtDES for M (8.6 +/- 0.8%) was statistically higher than for M0.5 (7.6 +/- 0.5%) and M1 (7.3 +/- 0.7%) protocols. Infusion of medetomidine reduces desflurane concentration required to maintain anaesthesia in dogs.     

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.