The influence of atipamezole on the cardiovascular effects of detomidine in horses

The reversal of the cardiovascular effects of the α₂-adrenoceptor agonist detomidine by the α₂-antagonist atipamezole was studied. Nine horses were given detomidine 20 μg/kg iv. On a separate occasion they were given atipamezole 100 μg/kg iv 15 mins after the detomidine injection. Blood gas tensions were measured and clinical signs of sedation were also observed. Bradycardia and the frequency of heart blocks induced by detomidine were reduced after atipamezole and blood pressure decreased. These reversal effects of atipamezole were of short duration (a few minutes) at the dose level tested. Two of the nine horses exhibited premature depolarisations after administration of detomidine, but not after atipamezole injection. PaO₂ decreased and PaCO₂ increased slightly after detomidine injection, but the arterial pH was within reference values or slightly elevated. Administration of atipamezole did not alter these values. Base excess rose after detomidine, and it decreased more quickly towards the baseline level, when the horses were given detomidine alone. No clinical adverse effects were seen from the administration of atipamezole. Atipamezole may be beneficial, if detomidine-induced bradycardia needs to be reversed in horses.     

Sedative and cardiovascular effects of romifidine, alone and in combination with butorphanol, in the horse

The behavioural and sedative effects of intravenous (iv) romifidine (40 and 80 μg/kg bodyweight [bwt]) alone or in combination with iv butorphanol (50 μg/kg bwt) were investigated in four ponies and one Thoroughbred horse. Apparent sedation, as judged by the lowering of the head, and by the response to imposed touch, visual and sound stimuli was assessed. The combination with butorphanol reduced the animals' response to imposed stimuli when compared with the effect of the same dose of romifidine alone. Following the administration of romifidine/butorphanol combinations muzzle tremor was noted and some animals attempted to walk forward. In a separate series, the cardiopulmonary effects of iv romifidine (80 μg/kg bwt) alone, or in combination with butorphanol (50 μg/kg bwt) were investigated. Romifidine and the romifidine/butorphanol combination caused similar cardiovascular changes, these being bradycardia with heart block, and hypertension followed by hypotension. Romifidine caused a transient decrease in arterial oxygen tensions and arterial carbon dioxide tensions had increased significantly by the end of the 90 min recording period. Romifidine/butorphanol combinations produced significantly higher arterial carbon dioxide tensions during the first 15 mins after drug administration than did romifidine alone. Butorphanol at 50 μg/kg bwt iv reduced the response to imposed stimuli in horses sedated with romifidine. The combination produced no cardiovascular changes beyond those induced by romifidine alone, but did increase the degree of respiratory depression.     

Medetomidine/ketamine sedation in calves and its reversal with atipamezole

Atipamezole was used to reverse the sedation induced in calves by medetomidine/ketamine. Thirteen claves subjected to umbilical surgery received medetomidine 20 μg/kg bodyweight (bwt) and ketamine 0.5 mg/kg bwt intravenously (iv) from a mixture of the drugs in one syringe. Atipamezole was given at doses of 20 to 60 μg/kg iv and intramuscularly (im) to the calves at the end of the operation. Following the administration of medetomidine and ketamine, PaCO₂ increased whereas pH, PaO₂ and heart rate decreased. Reversing the effects of medetomidine with atipamezole did not cause undesirable effects; recovery was rapid and smooth, most of the animals reached a standing position within 1 to 3 mins after the atipamezole injection.     

Detomidine: a new sedative for horses

Detomidine, given intravenously at doses of 5 to 30 (mean 13) micrograms/kg bodyweight (bwt), provided adequate sedation for a variety of clinical procedures in 93 per cent of administrations, and improved the ease of handling in the remaining animals. Side effects of ataxia and bradycardia were minimal at the lower dose rates. Higher doses were required for intramuscular use. In experimental trials 10 and 20 micrograms/kg bwt resulted in deep sedation and also significant hypertension and bradycardia of over 15 mins duration. Current literature on the use of detomidine in horses is reviewed.     

Prolonging dissociative anaesthesia in horses with a repeated bolus injection

The effects of prolonging romifidine/ketamine anaesthesia in horses with a second injection of ketamine alone or both romifidine/ketamine compared with only induction injection of romifidine and tiletamine/zolazepam were studied in 6 horses anaesthetised in lateral recumbency on 3 random occasions. All horses were sedated with romifidine 0.1 mg/kg bwt iv and, on 2 occasions, anaesthesia was induced by iv injection of ketamine 2.2 mg/kg bwt. To prolong the ketamine-induced anaesthesia, either ketamine (I.1 mg/kg bwt iv) or ketamine and romifidine (I.1 mg/kg bwt and 0.04 mg/kg bwt iv, respectively) were given 18–20 min after the start of the ketamine injection for induction. On the third occasion, anaesthesia was induced by iv injection of 1.4 mg/kg bwt Zoletil (0.7 mg/kg bwt tiletamhe + 0.7 mg/kg bwt zolazepam). No statistically significant differences in the measured cardiorespiratory function were found between the 3 groups. Heart rate was decreased significantly after sedation but increased during anaesthesia. Arterial blood pressure increased after sedation and remained high during anaesthesia. A significant decrease in arterial oxygen tension was observed in all groups during anaesthesia. The muscle relaxation induced by romifidine was, in most cases, not sufficient to abolish the catalepsy following a repeated injection of ketamine alone. Zoletil or a repeated injection of ketaminehornifidine resulted in smoother anaesthesia. When additional time is required to complete surgery during field anaesthesia, it is advisable to prolong romifidine/ketamine anaesthesia with an injection of both romifidine and ketamine in healthy horses. When a longer procedure is anticipated from the start Zoletil is an alternative for induction of anaesthesia. The mean time to response to noxious stimuli and mean time spent in lateral recumbency was 28 and 38 min for the anaesthesia prolonged with ketamine, 3.5 and 43 rnin for the anaesthesia prolonged with ketaminehornifidine and 33 and 45 min for the anaesthesia with Zoletil. All horses reached a standing position at the first attempt.     

Antagonism of Detomidine-Induced Sedation,Analgesia, Clinicophysiological,and Hematobiochemical Effects in Donkeys Using IV Tolazoline or Atipamezole

The present study aimed to investigate and evaluate the reversal of sedation, analgesia, ataxia, clinicophysiological findings, and hematobiochemical effects of detomidine by subsequent IV administration of tolazoline or atipamezole to improve safety and utility of detomidine in donkeys. Six mature donkeys weighing 250–300 kg and aged 4–6 years were used on three separate occasions. Each donkey received the following three treatments at the rate of one treatment per week in a randomized crossover study. The first group received 0.04 mg/kg bwt detomidine. The second group received 0.04 mg/kg bwt detomidine followed by 4.0 mg/kg bwt tolazoline. The third group received 0.04 mg/kg bwt detomidine followed by 0.4 mg/kg bwt atipamezole. Sedation, analgesia, ataxia, pulse rate, respiratory rate, and rectal temperature were recorded at 5 minutes before, then at 5, 15, 30, 60, and 90 minutes after injections. Red blood cell and white blood cell counts, Packed cell volume (%), hemoglobin, total protein, cholesterol, glucose, urea, aspartate amino transferase, alanine amino transferase, and gamma glutamyl transferase values were determined. Detomidine induced deep sedation, complete analgesia, and significant ataxia. Pulse and respiratory rates were decreased from the base line values, although rectal temperature was within the baseline value. The alterations in hematological and hematobiochemical parameters were mild and transient.     

Pharmacokinetics of detomidine and its metabolites following intravenous and intramuscular administration in horses

Reasons for performing study: Detomidine is commonly used i.v. for sedation and analgesia in horses, but the pharmacokinetics and metabolism of this drug have not been well described. Objectives: To describe the pharmacokinetics of detomidine and its metabolites, 3‐hydroxy‐detomidine (OH‐detomidine) and detomidine 3‐carboxylic acid (COOH‐detomidine), after i.v. and i.m. administration of a single dose to horses. Methods: Eight horses were used in a balanced crossover design study. In Phase 1, 4 horses received a single dose of i.v. detomidine, administered 30 μg/kg bwt and 4 a single dose i.m. 30 üg/kg bwt. In Phase 2, treatments were reversed. Plasma detomidine, OH‐detomidine and COOH‐detomidine were measured at predetermined time points using liquid chromatography‐mass spectrometry. Results: Following i.v. administration, detomidine was distributed rapidly and eliminated with a half‐life (t_1/2(el)) of approximately 30 min. Following i.m. administration, detomidine was distributed and eliminated with t_1/2(el) of approximately one hour. Following, i.v. administration, detomidine clearance had a mean, median and range of 12.41, 11.66 and 10.10–18.37 ml/min/kg bwt, respectively. Detomidine had a volume of distribution with the mean, median and range for i.v. administration of 470, 478 and 215–687 ml/kg bwt, respectively. OH‐detomidine was detected sooner than COOH‐detomidine; however, COOH‐detomidine had a much greater area under the curve. Conclusions and potential relevance: These pharmacokinetic parameters provide information necessary for determination of peak plasma concentrations and clearance of detomidine in mature horses. The results suggest that, when a longer duration of plasma concentration is warranted, the i.m. route should be considered.     

Assessment of the sedative effects of buprenorphine administered with 20 microg/kg detomidine in horses

The aim of this randomised, observer-blinded, crossover study was to compare the effects of four treatments, administered intravenously to six horses: saline and saline; 10 μg/kg detomidine and 7.5 μg/kg buprenorphine; 20 μg/kg detomidine and 7.5 μg/kg buprenorphine; and 20 μg/kg detomidine and 10 μg/kg buprenorphine. Sedation was subjectively assessed and recorded on a visual analogue scale. Peak sedation and duration of sedation were investigated using a univariate general linear model with post-hoc Tukey tests (P<0.05). Increasing the dose of detomidine from 10 to 20 μg/kg increased the degree of sedation when administered with the same dose of buprenorphine (7.5 μg/kg). When administered with 20 μg/kg detomidine, increasing the dose of buprenorphine from 7.5 to 10 μg/kg did not influence the degree of sedation achieved.     

Combined use of detomidine with opiates in the horse

The effects of administration of one of four opiates (pethidine 1 mg/kg bodyweight (bwt), morphine 0.1 mg/kg bwt, methadone 0.1 mg/kg bwt, and butorphanol 0.05 mg/kg bwt) given intravenously to horses and ponies already sedated with detomidine (10 micrograms/kg bwt) were investigated. Behavioural, cardiovascular and respiratory effects of the combinations were compared with those occurring with detomidine alone. Addition of the opiate increased the apparent sedation and decreased the response of the animal to external stimuli. At doses used, butorphanol produced the most reliable response. Side effects seen were increased ataxia (greatest following methadone and butorphanol) and excitement (usually muzzle tremors and muscle twitching). Following pethidine, generalised excitement was sometimes seen. Marked cardiovascular changes occurred in the first few minutes after morphine or pethidine injection, but within 5 mins cardiovascular changes were minimal. Following morphine or pethidine there was a significant increase in arterial carbon dioxide tension. Fourteen clinical cases were successfully sedated using detomidine/butorphanol combinations.     

Assessment of the sedative effects of buprenorphine administered with 10 μg/kg detomidine in horses

The aim of this randomised, observer-blinded, crossover study was to compare the effects of six treatments, administered intravenously to six horses: saline and saline (S/S); detomidine and saline (D/S); detomidine and 5 μg/kg buprenorphine (D/B5); detomidine and 7.5 μg/kg buprenorphine (D/B7.5); detomidine and 10 μg/kg buprenorphine (D/B10); and detomidine and 25 μg/kg butorphanol (D/BUT). The detomidine dose was 10 μg/kg for all treatments in which it was included. Sedation was subjectively assessed and recorded on a visual analogue scale. Peak sedation, duration of sedation and the area under the curve (AUC) for sedation scores were investigated using a univariate general linear model with post-hoc Tukey tests (P<0.05). Peak sedation and duration of sedation were statistically significantly different between treatments (P<0.001). No sedation was apparent after administration of S/S. The AUC was significantly different between treatments (P=0.010), with S/S being significantly different from D/S, D/BUT, D/B5 and D/B7.5, but not D/B10 (P=0.051).     

Plasma concentrations,behavioural and physiological effects following intravenous and intramuscular detomidine in horses

Reasons for performing study: Detomidine hydrochloride is used to provide sedation, muscle relaxation and analgesia in horses, but a lack of information pertaining to plasma concentration has limited the ability to correlate drug concentration with effect. Objectives: To build on previous information and assess detomidine for i.v. and i.m. use in horses by simultaneously assessing plasma drug concentrations, physiological parameters and behavioural characteristics. Hypothesis: Systemic effects would be seen following i.m. and i.v. detomidine administration and these effects would be positively correlated with plasma drug concentrations. Methods: Behavioural (e.g. head position) and physiological (e.g. heart rate) responses were recorded at fixed time points from 4 min to 24 h after i.m. or i.v. detomidine (30 μg/kg bwt) administration to 8 horses. Route of administration was assigned using a balanced crossover design. Blood was sampled at predetermined time points from 0.5 min to 48 h post administration for subsequent detomidine concentration measurements using liquid chromatography‐mass spectrometry. Data were summarised as mean ± s.d. for subsequent analysis of variance for repeated measures. Results: Plasma detomidine concentration peaked earlier (1.5 min vs. 1.5 h) and was significantly higher (105.4 ± 71.6 ng/ml vs. 6.9 ± 1.4 ng/ml) after i.v. vs. i.m. administration. Physiological and behavioural changes were of a greater magnitude and observed at earlier time points for i.v. vs. i.m. groups. For example, head position decreased from an average of 116 cm in both groups to a low value 35 ± 23 cm from the ground 10 min following i.v. detomidine and to 64 ± 24 cm 60 min after i.m. detomidine. Changes in heart rate followed a similar pattern; low value of 17 beats/min 10 min after i.v. administration and 29 beats/min 30 min after i.m. administration. Conclusions: Plasma drug concentration and measured effects were correlated positively and varied with route of administration following a single dose of detomidine. Potential relevance: Results support a significant influence of route of administration on desirable and undesirable drug effects that influence case management.     

A comparison of the efficacy of detornidine by sublingual and intramuscular administration in ponies

Preliminary trials established that, whilst detomidine is ineffective if given by stomach tube and is of variable efficacy in food, it can give effective sedation when administered by the sublingual route. A comparison was made in four ponies of the behavioural effects, and the effects on heart rate of detomidine at three dose rates (20, 40 and 80 μg/kg) given either by intramuscular injection or sublingually by squirting the drug under the tongue. Sedation was assessed by measuring the lowering of the ponies' heads and by scoring their responses to a variety of imposed stimuli. Ponies became sedated following detomidine administration at all doses and by all routes. The lowering of the head induced by detomidine was significantly influenced by the dose of drug and by the route of administration. For either route, higher doses produced the greatest effect. There was a significant correlation between the effects produced by the two routes of administration, the lowering of the head following sublingual administration being approximately threequarters of that after the same dose given intramuscularly. Onset of sedation was achieved more rapidly following intramuscular dosing than after sublingual administration. Falls in heart rate were similar after all drug administrations, but bradycardia was never profound. Subsequent clinical experience has proved that, providing adequate time (45 minutes) is allowed for maximal effects, sublingual administration of detomidine (40 μg/kg) can give a useful degree of sedation in horses which are difficult to inject.     

Changes in heart rate, mean arterial pressure, blood biochemistry, plasma glucose, plasma lactate and some plasma enzymes during sufentanil/halothane anaesthesia in horses

Nine horses were each anaesthetised for 40 min using SufentaniVhalothane. No surgery was performed. After premedication (detomidine 5 pgkg bwt iv) induction of anaesthesia was achieved by a combination of guaiphenesinlthiopentone. Anaesthesia was maintained by inhalation of halothane (0.8%) in oxygen. Six horses (Group 1) received 1 pgkg bwt sufentanil followed by a second injection (1 pg/kg bwt) after 20 min. Three horses (Group 2) received 2 pg/kg bwt sufentanil also followed by a second injection (2 pg/kg bwt) after 20 min. Each sufentanil injection produced a slight decrease in mean arterial blood pressure with a gradual return to the initial pressure. Bradycardia was also observed. Sufentanil injection induced apnoea needing artificial ventilation. Arterial blood was sampled for analysis during the anaesthetic procedure. At the end of anaesthesia, 1 h and 24 h after rising, venous blood was sampled to determine concentrations of lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and creatine phosphokinase (CPK). Values obtained were compared with values in blood taken before premedication. Plasma glucose and lactate concentrations just before sufentanil administration, at the end of anaesthesia and 1 h after rising were compared to control values. Plasma glucose concentration increased significantly during anaesthesia but returned to normal values 1 h after rising. All other parameters stayed within physiological ranges. In both groups spontaneous respiration returned 20–25 min after the second sufentanil injection. Recovery was uneventful.     

Sedation with detomidine and acepromazine influences the endoscopic evaluation of laryngeal function in horses

REASON FOR PERFORMING STUDY: Endoscopy of the upper airways of horses is used as a diagnostic tool and at purchase examinations. On some occasions it is necessary to use sedation during the procedure and it is often speculated that the result of the examination might be influenced due to the muscle-relaxing properties of the most commonly used sedatives. OBJECTIVES: To evaluate the effect of detomidine (0.01 mg/kg bwt) and acepromazine (0.05 mg/kg bwt) on the appearance of symmetry of rima glottidis, ability to abduct maximally the arytenoid cartilages and the effect on recurrent laryngeal neuropathy (RLN) grade. METHODS: Forty-two apparently normal horses underwent endoscopic examination of the upper airways on 3 different occasions, under the influence of 3 different treatments: no sedation (control), sedation with detomidine and sedation with acepromazine. All examinations were performed with a minimum of one week apart. The study was performed as an observer-blind cross-over study. RESULTS: Sedation with detomidine had a significant effect on the RLN grading (OR = 2.91) and ability maximally to abduct the left arytenoid cartilages (OR = 2.91). Sedation with acepromazine resulted in OR = 2.43 for the RLN grading and OR = 2.22 for the ability to abduct maximally. The ability to abduct maximally the right arytenoid cartilage was not altered. CONCLUSIONS: Sedating apparently healthy horses with detomidine or acepromazine significantly impairs these horses' ability to abduct fully the left but not the right arytenoid cartilage. This resulted in different diagnosis with respect to RLN when comparing sedation to no sedation. POTENTIAL RELEVANCE: Since the ability to abduct the right arytenoid cartilage fully is not altered by sedation, it is speculated that horses changing from normal to abnormal laryngeal function when sedated, might be horses in an early stage of the disease. To confirm or reject these speculations, further studies are needed. Until then sedation during endoscopy should be used with care.     

Plasma drug concentrations and clinical effects of a peripheral alpha‐2‐adrenoceptor antagonist,MK‐467, in horses sedated with detomidine

ObjectiveTo investigate plasma drug concentrations and the effect of MK-467 (L-659′066) on sedation, heart rate and gut motility in horses sedated with intravenous (IV) detomidine.Study designExperimental randomized blinded crossover study.AnimalsSix healthy horses.MethodsDetomidine (10 μg kg^?1 IV) was administered alone (DET) and in combination with MK-467 (250 μg kg^?1 IV; DET + MK). The level of sedation and intestinal sounds were scored. Heart rate (HR) and central venous pressure (CVP) were measured. Blood was collected to determine plasma drug concentrations. Repeated measures anova was used for HR, CVP and intestinal sounds, and the Student's t-test for pairwise comparisons between treatments for the area under the time-sedation curve (AUC_sed) and pharmacokinetic parameters. Significance was set at p < 0.05.ResultsA significant reduction in HR was detected after DET, and HR was significantly higher after DET + MK than DET alone. No heart blocks were detected in any DET + MK treated horses. DET + MK attenuated the early increase in CVP detected after DET, but later the CVP decreased with both treatments. Detomidine-induced intestinal hypomotility was prevented by MK-467. AUC_sed was significantly higher with DET than DET + MK, but maximal sedations scores did not differ significantly between treatments. MK-467 lowered the AUC of the plasma concentration of detomidine, and increased its volume of distribution and clearance.Conclusions and clinical relevanceMK-467 prevented detomidine induced bradycardia and intestinal hypomotility. MK-467 did not affect the clinical quality of detomidine-induced sedation, but the duration of the effect was reduced, which may have been caused by the effects of MK-467 on the plasma concentration of detomidine. MK-467 may be useful clinically in the prevention of certain peripheral side effects of detomidine in horses.     

The use of intraoperative fentanyl in spontaneously breathing dogs undergoing orthopaedic surgery

Nineteen dogs were assigned randomly to one of three groups. Animals in Group 1 were pre-medicated with acepromazine, 50 μg/kg bodyweight (bwt) intramuscularly (im) and received 10 ml of 0.9 per cent saline intravenously (iv) at the time of skin incision. Dogs in Group 2 were pre-medicated with acepromazine, 50 μg/kg bwt im, and received fentanyl 2 μg/kg bwt iv at skin incision. Dogs in Group 3 were pre-medicated with acepromazine, 50 μg/kg bwt and atropine, 30 to 40 μg/kg bwt, im and received fentanyl, 2 μg/kg bwt iv at skin incision. Pulse rate, mean arterial blood pressure, respiratory rate and end tidal carbon dioxide were measured before and after fentanyl or saline injection. Fentanyl caused a short-lived fall in arterial blood pressure that was significant in dogs premedicated with acepromazine, but not in dogs pre-medicated with acepromazine and atropine. A significant bradycardia was evident for 5 mins in both fentanyl treated groups. The effect on respiratory rate was most pronounced in Group 3, in which four of seven dogs required intermittent positive pressure ventilation (IPPV) for up to 14 mins. Two of six dogs in Group 2 required IPPV, whereas respiratory rate remained unaltered in the saline controls. The quality of anaesthesia was excellent in the fentanyl treated groups; however, caution is urged with the use of even low doses of fentanyl in spontaneously breathing dogs under halothane-nitrous oxide anaesthesia.     

The cardiorespiratory effects of morphine and butorphanol in horses anaesthetised under clinical conditions

Twenty-five horses admitted for minor orthopaedic or soft tissue surgery were anaesthetised with detomidine, ketamine and halothane. Heart rate, arterial blood pressure, respiratory rate, tidal volume, minute volume, blood gases and occlusion pressures were measured before and for 30 mins after intravenous (iv) injection of saline, butorphanol 0.05 mg/kg bodyweight (bwt) or morphine 0.02 or 0.05 mg/kg bwt. Drug or saline treatment induced no significant changes from pre-treatment values within a group for arterial blood pressure, heart rate, respiratory rate, arterial carbon dioxide tension, arterial oxygen tension and occlusion pressure. In conclusion, both morphine and butorphanol at the stated doses cause no adverse effects on the cardiovascular and respiratory systems of anaesthetised horses.     

The pharmacokinetics of ketamine after a continuous infusion under halothane anaesthesia in horses

The pharmacodynamics and pharmacokinetics of ketamine, when administered by infusion as an adjunct to halothane anaesthesia in horses, were investigated in 5 equine patients presented for routine castration. Anaesthesia was induced with detomidine, 20 μg/kg, followed by ketamine, 2.2 mg/kg bwt, the trachea intubated and the horses allowed to breathe halothane in oxygen. Five minutes later, a constant rate infusion of ketamine, 40 μg/kg min, was commenced and the halothane vaporiser concentration adjusted to maintain a light plane of anaesthesia. The mean infusion duration was 62 min (range 40–103). The ketamine was switched off approximately 15 min before the halothane. Plasma ketamine and norketamine levels, determined by high performance liquid chromatography, ranged from 0.74–2.04 μg/ml and 0.15–0.75 μg/ml, respectively, during the infusion period. The harmonic mean elimination half-life of ketamine was 46.1 min, mean volume of distribution at steady state (Vdss) was 1365 (271) ml/kg, mean body clearance (Cl) was 32.3 (9.1) ml/min.kg, and average mean residence time for the infusion (MRTinf) was 105.9 (20.4) min, respectively. Following termination of halothane, mean times to sternal recumbency and standing were 21.1 (6.9) and 41.6 (17.0) min, respectively. Surgical conditions were considered highly satisfactory, and physiological parameters were well preserved in most animals.     

Anaesthetic and cardiorespiratory effects of propofol at 10% for induction and 1% for maintenance of anaesthesia in horses

Reasons for performing study: Studies have demonstrated the clinical usefulness of propofol for anaesthesia in horses but the use of a concentrated solution requires further investigation. Objectives: To determine the anaesthetic and cardiorespiratory responses to a bolus injection of 10% propofol solution in mature horses. Methods: Three randomised crossover experimental trials were completed. Trial 1: 6 horses were selected randomly to receive 10% propofol (2, 4 or 8 mg/kg bwt i.v.). Trial 2: 6 horses received 1.1 mg/kg bwt i.v. xylazine before being assigned at random to receive one of 5 different doses (1–5 mg/kg bwt) of 10% propofol. Trial 3: 6 horses were sedated with xylazine (0.5 mg/kg bwt, i.v.) and assigned randomly to receive 10% propofol (3, 4 or 5 mg/kg bwt, i.v.); anaesthesia was maintained for 60 min using an infusion of 1% propofol (0.2‐0.4 mg/kg bwt/min). Cardiorespiratory data, the quality of anaesthesia, and times for induction, maintenance and recovery from anaesthesia and the number of attempts to stand were recorded. Results: Trial 1 was terminated after 2 horses had received each dose of 10% propofol. The quality of induction, anaesthesia and recovery from anaesthesia was judged to be unsatisfactory. Trial 2: 3 horses administered 1 mg/kg bwt and one administered 2 mg/kg bwt were not considered to be anaesthetised. Horses administered 3–5 mg/kg bwt i.v. propofol were anaesthetised for periods ranging from approximately 10–25 min. The PaO₂ was significantly decreased in horses administered 3–5 mg/kg bwt i.v. propofol. Trial 3: The quality of induction and recovery from anaesthesia were judged to be acceptable in all horses. Heart rate and rhythm, and arterial blood pressure were unchanged or decreased slightly during propofol infusion period. Conclusions: Anaesthesia can be induced with a 10% propofol solution and maintained with a 1% propofol solution in horses administered xylazine as preanaesthetic medication. Hypoventilation and hypoxaemia may occur following administration to mature horses. Potential relevance: Adequate preanaesthetic sedation and oxygen supplementation are required in horses anaesthetised with propofol.