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.     

An evaluation of the influence of medetomidine hydrochloride and atipamezole hydrochloride on the arrhythmogenic dose of epinephrine in dogs during halothane anesthesia.

Alterations in the arrhythmogenic dose of epinephrine (ADE) were determined following administration of medetomidine hydrochloride (750 micrograms/M2) and a saline placebo, or medetomidine hydrochloride (750 micrograms/M2), followed by specific medetomidine reversal agent, atipamezole hydrochloride (50 micrograms/kg) 20 min later, in halothane-anesthetized dogs (n = 6). ADE determinations were made prior to the administration of either treatment, 20 min and 4 h following medetomidine/saline or medetomidine/atipamezole administration. Epinephrine was infused for 3 min at increasing dose rates (2.5 and 5.0 micrograms/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached. The interinfusion interval was 20 min. There were no significant differences in the amount of epinephrine required to reach the arrhythmia criterion following the administration of either treatment. In addition, the ADE at each determination was not different between treatment groups. In this study, the administration of medetomidine to halothane-anesthetized dogs did not alter their arrhythmogenic response to infused epinephrine.     

Medetomidine/propofol anaesthesia for gastroduodenal endoscopy in dogs

This study was performed to evaluate clinically the level of analgesia obtained during fibre optic gastroduodenal examination with an anaesthetic regimen consisting of 1000 μg/m²b.s.a. medetomidine premedica-tion (equivalent to 30–50 μg/kg b.w, IM) followed by induction and maintenance of anaesthesia with propofol (1–2 mg/kg, IV), with spontaneous respiration of room air. Following premedication, all the dogs (n=20) were connected to an E.C.G. monitor (lead II) and a femoral artery catheter was placed for continuous recording of blood pressure and to allow sampling for arterial blood gas analysis. The mean values for heart rate and arterial blood pressure following medetomidine administration were 55 b.p.m. and 121 mm Hg, respectively, and these values remained unchanged during the procedure. Blood gas data all remained within physiological limits. Fibre optic gastroduodenoscopy could be performed without the occurrence of “pain” responses. In all but one dog, the pyloric sphincter was relaxed and it was easy to pass the endoscope into the duodenum. All the dogs recovered rapidly and smoothly from anaesthesia, following administration of atipamezole 2500 μg/m² b.s.a. (equivalent to 75–125 μg/kg b.w.) IM to reverse the effects of the medetomidine.     

Anesthesia of captive African wild dogs (Lycaon pictus) using a medetomidine-ketamine-atropine combination.

Seven captive male African wild dogs (Lycaon pictus) weighing 25-32 kg each, were anesthetized by i.m. injection via hand syringe with a combination of 1.5 mg/kg ketamine, 40 microg/kg medetomidine, and 0.05 mg/kg atropine. Following endotracheal intubation, each animal was connected to a bain closed-circuit system that delivered 1.5% isoflurane and 2 L/min oxygen. Atipamezole (0.1 mg/kg i.v.; 0.1 mg/kg i.m.) was given at the end of each procedure (60 min following injection of medetomidine/ketamine/atropine). Time to sternal recumbency was 5-8 min. Times to standing after atipamezole administration were 8-20 min. This anesthetic regimen was repeated on three separate occasions (September 2000, February 2002, and October 2002) on all males to perform electroejaculation procedures. Each procedure was <80 min from injection to standing. Dogs showed excellent muscle relaxation during the procedures. Arterial blood samples were collected at 10-min intervals for blood gases in one procedure (September 2000). Separate venous samples were taken from each dog during each procedure for hematology and biochemistry. These values were within the normal range for this species. Arterial hemoglobin oxygen saturation (SpO2) and heart rate (HR) were monitored continuously in addition to other anesthesia monitoring procedures (body temperature, respiratory rate [RR], capillary refill time, blink response, pupil position, deep pain perception reflex). All dogs maintained relatively stable SpO2 profiles during monitoring, with a mean (+/-SD) SpO2 of 92% +/-5.4%. All other physiological variables (HR, RR, body temperature, blood pressure) were within normal limits. Following each procedure, normal behavior was noted in all dogs. All the dogs were reunited into the pack at completion of their anesthetic procedures. An injectable medetomidine-ketamine-atropine combination with maintenance by gaseous isoflurane and oxygen provides an inexpensive, reliable anesthetic for captive African wild dogs.     

The suitability of medetomidine sedation for intradermal skin testing in dogs

The objective of this study was to determine the suitability of medetomidine sedation for facilitating intradermal skin testing in dogs. Quality of sedation and immobilization, and effects of sedation on responses to intradermally injected histamine were evaluated. Ten clinically normal dogs were injected intradermally before and after medetomidine sedation (10 μg kg^?1 intravenously) with diminishing concentrations of histamine (100–10^?5μg mL^?1) and a negative control. Mean wheal responses at injection sites were compared before and during sedation, and no significant suppression of responses occurred during sedation. Medetomidine produced sedation that notably increased the ease of performing multiple intradermal injections in all dogs and sedative effects were rapidly reversed by the antagonist atipamezole. It was concluded that medetomidine may be an excellent sedative for facilitating intradermal skin testing in dogs provided further studies similarly reveal no inhibition of responses to intradermally injected allergens in atopic dogs.     

The effect of medetomidine premedication upon propofol induction and infusion anaesthesia in the dog

The effect of premedication with four different intramuscular doses of medetomidine (5.0,10.0, 20.0 and 40.0 μg.kg-¹) and a saline placebo were compared in a group of six adult beagle dogs anaesthetised with propofol on five separate occasions. Anaesthesia was induced 30 minutes after premedication and maintained by intravenous injection and continuous infusion of propofol. The effects of medetomidine were reversed with atipamezole 30 minutes after anaesthetic induction. The marked synergistic effects of medetomidine with propofol were demonstrated by a dose related reduction in the induction and infusion requirements for a similar degree of anaesthesia. The effect appeared exponential in nature; lower medetomidine doses produced a disproportionately greater effect.
The maintenance of anaesthesia with propofol following a saline placebo or low doses of medetomidine proved to be difficult. Higher doses of medetomidine required less propofol for induction and infusion and allowed a more stable anaesthesia to be maintained. Propofol produced no statistically significant change in heart rate during infusion. Changes in respiratory rate were markedly group specific. A significant reduction in respiratory rate was seen in dogs given either 5 μg.kg- or 10 μ-g.kg-¹ medetomidine. No change was recorded in dogs given 20 /μg.kg-¹ medetomidine and a significant increase was seen in dogs given 40 μg.kg-¹ medetomidine. Recovery was monitored following the termination of propofol infusion after the reversal of medetomidine using atipamezole at five times the medetomidine dose. Recovery was slower for dogs given lower doses of medetomidine and consequently higher doses of propofol.     

Medetomidine, a new sedative-analgesic for use in the dog and its reversal with atipamezole

The sedative and physiological effects of intramuscular medetomidine (20 and 40 μg/kg) in dogs were compared with those of xylazine (2 mg/kg). The efficacy of atipamezole (200 μg/kg), as an antagonist given 15 or 45 minutes after medetomidine (40 μg/kg) was studied. Following medetomidine, onset of sedation was rapid, and depth and duration of sedation were dose dependent. The higher dose produced jaw relaxation, depression of the pedal reflex, downward rotation of the eye and dogs could be positioned for radiography of the hips. Side effects were similar after either medetomidine or xylazine, and included bradycardia, a fall in respiratory rate and muscle tremor. Vomiting during induction was less frequent after medetomidine than after xylazine. Intramuscular administration of atipamezole rapidly reversed the sedative effects of medetomidine. Signs of arousal were seen within three minutes; all dogs could stand within 10 minutes and appeared clinically normal. Heart and respiratory rates rose, but did not return to presedation values. Relapse to sedation was not noted.     

Evaluation of the clinical efficacy and safety of intramuscular and intravenous doses of dexmedetomidine and medetomidine in dogs and their reversal with atipamezole

Two hundred and twelve dogs were treated either intravenously or intramuscularly with either dexmedetomidine or medetomidine in a randomised double-blinded multicentre clinical study during procedures such as dental care, radiography and otitis treatment. Sedative, analgesic and cardiorespiratory parameters and body temperature were assessed for three hours after the treatments. Approximately half the dogs were given atipamezole intramuscularly after the completion of the procedure, and the other dogs were allowed to recover spontaneously. Dexmedetomidine and medetomidine induced similar clinical effects, and the procedure was completed successfully in 97 per cent of cases. There were few adverse side effects, but they included prolonged sedation, hypothermia, apnoea and bradycardia; no adverse effects were observed after the administration of atipamezole, which effectively reversed all the clinical effects of dexmedetomidine and medetomidine.     

Actions and pharmacokinetic properties of the α2-adrenergic agents, medetomidine and atipamezole, in rainbow trout (Oncorhynchus mykiss)

The effects of medetomidine and atipamezole were examined in rainbow trout. Medetomidine proved to be an effective sedative but not an anaesthetic; its effects were antagonised by atipamezole. The clinical signs of medetomidine sedation were rapid settling to the bottom of the tank followed by progressive ataxia. The sedative effect was dose-dependent: at 1 mg/l, one of 6 fish rested on its side after 10 min, whereas at 20 mg/l all 6 rested on their sides. No loss of consciousness occurred. Atipamezole at 6 times the medetomidine concentration antagonised sedation. The average time before fish exposed to medetomidine alone showed avoidance reactions was 10 h, more than 5 times longer than the mean time in fish exposed to medetomidine and then atipamezole. During exposure to medetomidine (5 mg/l) opercular movement rate decreased from 80/min to 20/min. The nature of opercular excursions also changed from being rapid and shallow to slow and deep. Respiratory movements increased after transfer to the bath containing atipamezole. Medetomidine had a marked effect upon skin colour, with fish becoming very pale a few min after exposure. Normal pigmentation was not restored until 4.5 days after exposure to medetomidine alone, but returned to normal after 10 min exposure to atipamezole solution. The half-life (t¹/₂ lambda_z) for medetomidine was 5.5 h. For atipamezole, it was 8.6 h.     

Effects of medetomidine premedication on propofol infusion anaesthesia in dogs

Observations of cardiovascular and respiratory parameters were made on six dogs anaesthetized on two separate occasions for 120 minutes with a propofol infusion, once without premedication and once following premedication with 10 μg kg-¹ of intramuscular medetomidine. During anaesthesia the heart rate and cardiac index tended to be lower following medetomidine premedication, while the mean arterial pressure was significantly greater (p<0.05). Although the differences were not statistically significant, the systemic vascular resistance, pulmonary vascular resistance and stroke volume index were also greater in dogs given medetomidine. The mean arterial oxygen and carbon dioxide tensions were similar under both regimens, but in 2 dogs supplementary oxygen had to be administered during anaesthesia to alleviate severe hypoxaemia on both occasions they were anaesthetized. Minute and tidal volumes of respiration tended to be greater in dogs not given medetomidine but medetomidine premedication appeared to have no effect on venous admixture. Dogs given medetomidine received intramuscular atipamezole at the end of the 120 min. propofol infusion; the mean time from induction of anaesthesia to walking without ataxia was 174. min in the unpremedicated dogs and 160 min. in the dogs given atipamezole. The mean blood propofol concentration at which the dogs walked without ataxia was higher in the unpremedicated animals (2.12 ± 0.077 μg. ml-¹ compared with 1.27 ± 0.518 μg. ml-¹ in the premedicated dogs). The oxygen delivery to the tissues was lower after medetomidine premedication (p = 0.03) and the oxygen consumption was generally lower after medetomidine premedication but the difference did not achieve statistical significance. No correlation could be demonstrated between blood propofol concentration and cardiac index, systemic or pulmonary vascular resistance indices, systolic, diastolic or mean arterial blood pressures.     

Evaluation of two sedation protocols for use before diagnostic intra-articular anaesthesia in lame dogs

Objectives : To assess the influence of two sedation protocols on the degree of lameness in dogs. Methods : Fifty lame dogs were allocated to one of two sedation protocols. Group ACPM (acepromazine + methadone; n=25) was sedated with acepromazine and methadone. Group MED (medetomidine antagonised with atipamezole; n=25) was sedated with medetomidine and reversed with atipamezole. Each dog was evaluated for lameness before and after sedation using videotapes. Four experienced clinicians allocated global lameness scores before and after sedation to each dog using a numerical rating scale. Results : In 80% of the dogs in group ACPM and in 72% in group MED lameness was not affected by the sedation. In 12% of the dogs in group ACPM and 20% of the dogs in group MED the observers noticed an increase of lameness of 1 or 2 degrees on a scale of 0 to 10. In 8% of the dogs in both groups lameness decreased with 1 degree. Clinical Relevance : A possible diagnostic test for investigation of obscure lameness is intra‐articular anaesthesia. Sedation is necessary to allow intra‐articular injection. This study provided evidence that the effect of sedation with the proposed protocols on the degree of lameness is negligible.     

The cardiovascular and respiratory effects of medetomidine and thiopentone anaesthesia in dogs breathing at an altitude of 1486 m

The purpose of this study was to evaluate the cardio-respiratory effects of the combination of medetomidine and thiopentone followed by reversal with atipamezole as a combination for anaesthesia in 10 healthy German Shepherd dogs breathing spontaneously in a room at an altitude of 1486 m above sea level with an ambient air pressure of 651 mmHg. After the placement of intravenous and intra-arterial catheters, baseline samples were collected. Medetomidine (0.010 mg/kg) was administered intravenously and blood pressure and heart rate were recorded every minute for 5 minutes. Thiopentone was then slowly administered until intubation conditions were ideal. An endotracheal tube was placed and the dogs breathed room air spontaneously. Blood pressure, pulse oximetry, respiratory and heart rate, capnography, blood gas analysis and arterial lactate were performed or recorded every 10 minutes for the duration of the trial. Thiopentone was administered to maintain anaesthesia. After 60 minutes, atipamezole (0.025 mg/kg) was given intramuscularly. Data were recorded for the next 30 minutes. A dose of 8.7 mg/kg of thiopentone was required to anaesthetise the dogs after the administration of 0.010 mg/kg of medetomidine. Heart rate decreased from 96.7 at baseline to 38.5 5 minutes after the administration of medetomidine (P < 0.05). Heart rate then increased with the administration of thiopentone to 103.2 (P < 0.05). Blood pressure increased from 169.4/86.2 mmHg to 253.2/143.0 mmHg 5 minutes after the administration of medetomidine (P < 0.05). Blood pressure then slowly returned towards normal. Heart rate and blood pressure returned to baseline values after the administration of atipamezole. Arterial oxygen tension decreased from baseline levels (84.1 mmHg) to 57.8 mmHg after the administration of medetomidine and thiopentone (P < 0.05). This was accompanied by arterial desaturation from 94.7 to 79.7% (P < 0.05). A decrease in respiratory rate from 71.8 bpm to 12.2 bpm was seen during the same period. Respiratory rates slowly increased over the next hour to 27.0 bpm and a further increases 51.4 bpm after the administration of atipamezole was seen (P < 0.05). This was maintained until the end of the observation period. Arterial oxygen tension slowly returned towards normal over the observation period. No significant changes in blood lactate were seen. No correlation was found between arterial saturation as determined by blood gas analysis and pulse oximetry. Recovery after the administration of atipamezole was rapid (5.9 minutes). In healthy dogs, anaesthesia can be maintained with a combination of medetomidine and thiopentone, significant anaesthetic sparing effects have been noted and recovery from anaesthesia is not unduly delayed. Hypoxaemia may be problematic. Appropriate monitoring should be done and oxygen supplementation and ventilatory support should be available. A poor correlation between SpO2 and SaO2 and ETCO2 and PaCO2 was found.     

Atipamezole increases medetomidine clearance in the dog: an agonist—antagonist interaction

Medetomidine, an α₂-adrenoceptor agonist, is a potent sedative and analgesic agent in the dog. When necessary, its action can be effectively antagonized by atipamezole. The present work was designed to study the effects of these drugs on each others' pharmacokinetics when a single intramuscular dose of medetomidine (50 μg kg^-1) was followed by a dose of atipamezole (250 μg kg^-1). Three different treatments were used: medetomidine alone, atipamezole alone, and atipamezole after medetomidine. Drug concentrations in plasma were measured by GC-MS. Statistical analysis of the results (anova) revealed significant differences between treatments in the kinetic parameters of medetomidine. Atipamezole decreased the AUC of medetomidine from 41.3 to 28.6 ng h ml"¹(P = 0.005), t_1/4 from 1.44 to 0.87 h ( P = 0.015), and increased Cl from 21 to 31 ml min^-1kg^-1(P = 0.017). Differences in V₂ did not reach statistical significance. The only statistically significant effects of medetomidine on the pharmacokinetics of atipamezole in this study were the slight decrease of Cl and C _max as well as the increase of AUC . It is suggested that the large dose of medetomidine used caused haemodynamic changes, resulting in decreased hepatic circulation and slower drug metabolism. Antagonism by atipamezole restored the hepatic blood flow and, consequently, increased the elimination of medetomidine by biotransformation.     

Medetomidine as a premedicant in dogs and its reversal by atipamezole

Medetomidine (10, 20, 40 μg/kg) was used as a premedicant before thiopentone, halothane and nitrous oxide anaesthesia in 60 dogs undergoing a variety of elective surgical and diagnostic procedures at the University of Liverpool Small Animal Hospital. The efficacy of the sedation produced by the three dose groups was evaluated using a sedation scoring system which is presented. Induction of anaesthesia was accomplished using 1–25 per cent thiopentone sodium administered slowly to effect. The mean dose of thiopentone required for intubation following 10 μ-g/kg medetomidine (group 1) was 6–9 mg/kg (SD ± 2–3 mg/kg), following 20 μ-g/kg medetomidine (group 2) was 4–5 mg/kg (SD ± 1–6 mg/kg) and following 40 μg/kg (group 3) was 2–4 mg/kg (SD ± 2–5 mg/kg). Induction of anaesthesia was generally smooth and significant apnoea (greater than 45 seconds) was not noted. Anaesthesia was maintained in all cases using halothane vapourised in a one part oxygen to two parts nitrous oxide mixture, delivered to the patient via a suitable non-breathing circuit (Magill, Bain or T Piece). At the conclusion of the procedure, atipamezole (50, 100, 200 μg/kg) was administered intramuscularly to half of the dogs in each group (10 dogs). Dogs receiving atipamezole recovered rapidly and smoothly to sternal recumbency, group 1 taking 8-5 minutes (SD ± 2–7 minutes), group 2 taking 11-8 minutes (SD ± 3–6 minutes), and group 3 taking 12-6 minutes (sd ± 4–5 minutes). When atipamezole was not administered a dose dependent increase in recumbency time occurred.     

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.     

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.     

The effects of topical tropicamide and systemic medetomidine, followed by atipamezole reversal, on pupil size and intraocular pressure in normal dogs

Twenty normal Golden Retrievers being screeened for eye, hip and elbow diseases were given tropicamide topically and medetomidine systemically. Medetomidine effects were later reversed with systemic atipamezole. Pupil size and intraocular pressure changes were determined. Pupil size increased significantly following tropicamide administration and continued to increase slightly but significantly after medetomidine injection. It was unclear whether the slight increase in pupil size following medetomidine administration was due to continued effect of tropicamide or due to the medetomidine itself. Atipamezole did not influence pupil size. Intraocular pressure (IOP) was not affected by these drugs. Ophthalmic screening examination for inherited disease following tropicamide administration is equally feasible prior to sedation with medetomidine and after reversal with atipamezole, but not during the period of sedation.     

Effects of medetomidine on intestinal and colonic motility in the dog

The motor responses of the jejunum and colon to stimulation of α₂-adrenoceptors by medetomidine and clonidine were investigated in four dogs. In fasting dogs, medetomidine, at a dose rate of 30 μg/kg i.v., disrupted the migrating myoelectric complex (MMC) pattern of the small intestine for about 2 h. Similar, but shorter-lasting effects were also induced by clonidine (30 μg/kg i.v.) on the jejunum. The administration of α₂-agonists inhibited colonic motility in fasting dogs, although medetomidine-induced inhibition was preceded by a short period of increased muscle tone. All these effects were reversed by the α₂-antagonists atipamezole (0.15 mg/kg i.v.) and yohimbine (0.20 mg/kg i.v.). In fed dogs, medetomidine (30 μg/kg i.v.) induced a strong increase of the tone on the proximal colon, while the activity of the medium and distal colon was completely suppressed. Yohimbine (0.50 mg/kg i.v.) immediately restored the activity of the colon and induced a propagated giant contraction and defaecation by the animal. These data confirm the importance of a₂-adrenergic receptors in the control of intestinal and colonic motility in the dog.     

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.     

Reversal of medetomidine-induced sedation in reindeer (Rangifer tarandus tarandus) with atipamezole increases the medetomidine concentration in plasma

The pharmacokinetics of two potent α₂-adrenoceptor agents that can be used for immobilization (medetomidine) and reversal (atipamezole) of the sedation in mammals, were studied in three reindeer ( Rangifer tarandus tarandus) in winter and again in summer. Medetomidine (60 μg/kg) was injected intravenously (i.v.), followed by atipamezole (300 μg/kg) intravenously 60 min later. Drug concentrations in plasma were measured by HPLC. The administration of atipamezole resulted in an immediate 2.5–3.5 fold increase in the medetomidine concentration in plasma. Clearance for medetomidine (median 19.3 mL/min·kg) was lower than clearance for atipamezole (median 31.0 mL/min·kg). The median elimination half-lives of medetomidine and atipamezole in plasma were 76.1 and 59.9 min, respectively. The animals became resedated 0.5–1 h after the reversal with atipamezole. Resedation may be explained by the longer elimination half-life of medetomidine compared to atipamezole.