The sedative and analgesic effects of detomidine-butorphanol and detomidine alone in donkeys

Butorphanol and detomidine constitute an effective combination for sedation and analgesia in horses. This trial was undertaken to assess the effectiveness of this combination in donkeys. The detomidine and butorphanol were given intravenously one after the other. A dose of 10 microg/kg of detomidine and 25 microg/kg of butorphanol was used. Sedation is easily extended by additional doses of butorphanol. The average dose of detomidine was 11.24 microg/kg and that of butorphanol was 28.0 microg/kg. Four donkeys in the detomidine group required additional sedation and analgesia. Detomidine alone did not totally eliminate coronary band pain. Heart rates dropped significantly in the first minute after the injection of the combination. One donkey developed an atrioventricular block, while another developed a sino-atrial block. Four donkeys developed a Cheyne-Stokes respiratory pattern. The combination of detomidine and butorphanol is an effective combination for sedation and analgesia of donkeys for standing procedures.     

Standing sedation in captive zebra (Equus grevyi and Equus burchellii)

Nine Grevy's zebras (Equus grevyi) and three Burchell's zebras (Equus burchellii) were immobilized in a standing position a total of 70 times for minor, nonpainful procedures over a 9-yr period. Standing sedation was successfully obtained with a combination of detomidine and butorphanol on 47 occasions (67.1%). Detomidine i.m. (median 0.10 mg/kg; range: 0.07-0.21) was administered by dart, followed 10 min later by butorphanol i.m. (median 0.13 mg/kg; range 0.04-0.24). The dosages were varied depending on the initial demeanor of the animal. On 23 occasions (32.9%), small amounts of etorphine (median 2.5 microg/kg; range 1.1-12.3 microg/kg) plus acepromazine (median 10 microg/kg; range 4.4-50 microg/kg) (as in Large Animal-Immobilon) had to be administered i.m. to gain sufficient sedation. In these latter cases, the animals were either excited or known for their aggressive character. The zebras were sufficiently immobilized for the length of most procedures (<45 min) without supplementation. At the end of the procedure, the animals were given atipamezole (2 mg per 1 mg detomidine used) and naltrexone (0.1 mg/kg) to reverse the sedative effects, irrespective of whether etorphine was used or not. Standing sedation, using the combination of the alpha-2 agonist detomidine and the partial agonist-antagonist opioid butorphanol (in some cases supplemented with etorphine + acepromazine), proved to be a very efficacious and safe method to be used in zebras under zoo conditions for short-lasting, nonpainful procedures.     

A comparison of ketorolac with flunixin, butorphanol, and oxymorphone in controlling postoperative pain in dogs.

Ketorolac tromethamine, a nonsteroidal anti-inflammatory analgesic, was compared with flunixin and butorphanol for its analgesic efficacy and potential side effects after laparotomy or shoulder arthrotomy in dogs. Sixty-four dogs were randomly assigned to receive butorphanol 0.4 mg/kg body weight (BW) (n = 21), flunixin 1.0 mg/kg BW (n = 21), or ketorolac 0.5 mg/kg BW (n = 22), in a double blind fashion. The analgesic efficacy was rated from 1 to 4 (1 = inadequate, 4 = excellent) for each dog. The average scores after laparotomy were ketorolac, 3.4; flunixin, 2.7; and butorphanol, 1.6. After shoulder arthrotomy, the average scores were ketorolac, 3.5; flunixin, 3.0; and butorphanol, 1.4 (5/11 dogs). As butorphanol was unable to control pain after shoulder arthrotomy, oxymorphone, 0.05 mg/kg BW, replaced butorphanol in a subsequent group of dogs and had a score of 2.0 (6/11 dogs). Serum alanine aminotransferase and creatinine were significantly elevated above baseline at 24 hours postoperatively in dogs receiving flunixin. One dog in each group developed melena or hematochezia. One dog receiving ketorolac had histological evidence of gastric ulceration. We concluded that ketorolac is a good analgesic for postoperative pain in dogs.     

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.     

Retrospective analysis of detomidine infusion for standing chemical restraint in 51 horses

Objective To assess the effectiveness of a detomidine infusion technique to provide standing chemical restraint in the horse. Design Retrospective study. Animals Fifty‐one adult horses aged 9.5 ± 6.9 years (range 1–23 years) and weighing 575 ± 290.3 kg. Methods Records of horses presented to our clinic over a 3‐year period in which a detomidine infusion was used to provide standing chemical restraint were reviewed. Information relating to the types of procedure performed, duration of infusion, drug dosages and adjunct drugs administered was retrieved. Results Detomidine was administered as an initial bolus loading dose (mean ± SD) of 7.5 ± 1.87 µg kg^?1. The initial infusion rate was 0.6 µg kg^?1 minute^?1, and this was halved every 15 minutes. The duration of the infusion ranged from 20 to 135 minutes. Twenty horses received additional detomidine or butorphanol during the procedure. All horses undergoing surgery received local anesthesia or epidural analgesia in addition to the detomidine infusion. A wide variety of procedures were performed in these horses. Conclusions Detomidine administered by infusion provides prolonged periods of chemical restraint in standing horses. Supplemental sedatives or analgesics may be needed in horses undergoing surgery. Clinical relevance An effective method that provides prolonged periods of chemical restraint in standing horses is described. The infusion alone did not provide sufficient analgesia for surgery and a significant proportion of animals required supplemental sedatives and analgesics.     

Detomidine-diazepam-ketamine anaesthesia in buffalo (Bubalus bubalis) calves

Eight buffalo calves (8-12 months, 70-100 kg) were randomly assigned to two groups of four animals each. Animals of group I were given detomidine (100 micrograms/kg), whereas animals of group II received a mixture of detomidine (100 micrograms/kg), diazepam (100 micrograms/kg) and ketamine (3 mg/kg) (DDK) intravenously. Various clinical parameters, such as weak time, down time, pedal and pinprick reflexes, muscle relaxation and extent of sedation, as well as heart and respiratory rates and electrocardiograms were measured before (time 0) and 15, 30, 45, 60, 75 and 90 min after treatment. In all the animals of group II (DDK), the pedal reflex was completely abolished (score: 3.00 +/- 0.00) within 5 min, the pinprick response was either very weak or it was completely abolished at this interval. Muscle relaxation and sedation were excellent within 5 min of DDK administration. The depth of sedation and analgesia was maximum from 5 to 15 min postinjection. Detomidine alone, however, failed to produce appropriate depression of the pedal and pinprick reflexes, sedation was mild and muscle relaxation was inadequate. Heart rate showed a significant (P < 0.05) decrease in group I, but the decrease was non-significant in group II. A more pronounced increase in respiratory rate was observed in group I as compared to group II. Animals of both groups recovered within 90 min without any complication. Minimal changes in the cardiovascular system in the group given the DDK combination were an advantage over the group given detomidine. The results indicated that DDK combination is safe and suitable for 15 min of anaesthesia with excellent muscle relaxation and has only limited cardiorespiratory effects in buffaloes.     

Electroencephalographic and cardiovascular variables as nociceptive indicators in isoflurane-anaesthetized horses

OBJECTIVE: To evaluate Fourier-transformed electroencephalographic (EEG) variables, mean arterial blood pressure (MAP) and pulse rate as nociceptive indicators in isoflurane-anaesthetized horses. ANIMALS: Five standardbred and three Norwegian cold-blooded trotter stallions undergoing castration, aged 2-4 years, mass 378-538 kg. MATERIALS AND METHODS: All horses received intravenous (IV) detomidine (10 microg kg(-1) IV) and butorphanol (0.01 mg kg(-1) IV). Additional detomidine (4 microg kg(-1) IV) was administered in the induction area. Anaesthesia was induced with ketamine (2.5 mg kg(-1) IV) and diazepam (40 microg kg(-1) IV), and maintained for 30 minutes with isoflurane (end-tidal concentration of 1.4%) vaporized in oxygen. The electroencephalogram, MAP and pulse rate were recorded for 15 minutes, beginning 5 minutes before skin incision. Differences between the mean values of recordings taken before, and during surgery were calculated and tested for significant differences using a two-sided Student's t-test. RESULTS: A significant rise in MAP and a fall in pulse rate were found. No significant change was found in any EEG variable. CONCLUSION/CLINICAL relevance Of the variables evaluated, MAP seems to be the most sensitive and reliable indicator of nociception in isoflurane-anaesthetized horses.     

Effect of detomidine on visceral and somatic nociception and duodenal motility in conscious adult horses

ObjectiveTo evaluate the effects of detomidine on visceral and somatic nociception, heart and respiratory rates, sedation, and duodenal motility and to correlate these effects with serum detomidine concentrations.Study designNonrandomized, experimental trial.AnimalsFive adult horses, each with a permanent gastric cannula weighing 534 ± 46 kg.MethodsVisceral nociception was evaluated by colorectal (CRD) and duodenal distension (DD). The duodenal balloon was used to assess motility. Somatic nociception was assessed via thermal threshold (TT). Nose–to–ground (NTG) height was used as a measure of sedation. Serum was collected for pharmacokinetic analysis. Detomidine (10 or 20 μg kg^?1) was administered intravenously. Data were analyzed by means of a three–factor anova with fixed factors of treatment and time and random factor of horse. When a significant time × treatment interaction was detected, differences were compared with a simple t–test or Bonferroni t–test. Significance was set at p < 0.05.ResultsDetomidine produced a significant, dose–dependent decrease in NTG height, heart rate, and skin temperature and a significant, nondose–dependent decrease in respiratory rate. Colorectal distension threshold was significantly increased with 10 μg kg^?1 for 15 minutes and for at least 165 minutes with 20 μg kg^?1. Duodenal distension threshold was significantly increased at 15 minutes for the 20 μg kg^?1 dose. A significant change in TT was not observed at either dose. A marked, immediate decrease in amplitude of duodenal contractions followed detomidine administration at both doses for 50 minutes.Conclusions and clinical relevanceDetomidine caused a longer period of visceral anti–nociception as determined by CRD but a shorter period of anti–nociception as determined by DD than has been previously reported. The lack of somatic anti–nociception as determined by TT testing may be related to the marked decrease in skin temperature, likely caused by peripheral vasoconstriction and the low temperature cut–off of the testing device.     

Preliminary study of the effects of xylazine or detomidine with or without butorphanol for standing sedation in dairy cattle

The sedative effect induced by administering xylazine hydrochloride or detomidine hydrochloride with or without butorphanol tartrate to standing dairy cattle was compared in two groups of six adult, healthy Holstein cows. One group received xylazine (0.02 mg/kg i.v.) followed by xylazine (0.02 mg/kg) and butorphanol (0.05 mg/kg i.v.) 1 week later. Cows in Group B received detomidine (0.01 mg/kg i.v.) followed by detomidine (0.01 mg/kg i.v.) and butorphanol (0.05 mg/kg i.v.) 1 week later. Heart rate, respiratory rate, and arterial blood pressure were monitored and recorded before drugs were administered and every 10 minutes for 1 hour after drug administration. The degree of sedation was evaluated and graded. Cows in each treatment group had significant decreases in heart rate and respiratory rate after test drugs were given. Durations of sedation were 49.0 +/- 12.7 minutes (xylazine), 36.0 +/- 14.1 (xylazine with butorphanol), 47.0 +/- 8.1 minutes (detomidine), and 43.0 +/- 14.0 minutes (detomidine with butorphanol). Ptosis and salivation were observed in cows of all groups following drug administration. Slow horizontal nystagmus was observed from three cows following administration of detomidine and butorphanol. All cows remained standing while sedated. The degree of sedation seemed to be most profound in cows receiving detomidine and least profound in cows receiving xylazine.     

Evaluation of the sedative,analgesic, clinicophysiological and haematological effects of intravenous detomidine,detomidine‐butorphanol,romifidine and romifidine‐butorphanol in standing donkeys

The aim of this investigation was to determine and evaluate the sedative, analgesic, clinicophysiological and haematological effects of intravenous (i.v.) injection of detomidine, detomidine‐butorphanol, romifidine and romifidine‐butorphanol. Six standing donkeys were used. Each donkey received 4 i.v. treatments and the order of treatment was randomised with a one‐week interval between each treatment. We found that i.v. injection of a combination of detomidine‐butorphanol or romifidine‐butorphanol produced potent neuroleptanalgesic effects thus providing better, safe and effective sedation with complete analgesia in standing donkeys compared with injection of detomidine or romifidine alone. The changes and reduction in pulse rate were within acceptable limits. The changes in clinicophysiological, haematological and biochemical values were mild and transient in these clinically healthy donkeys.     

Standing sedation in African elephants (Loxodonta africana) using detomidine-butorphanol combinations.

Standing sedation was provided for 14 clinical procedures in three African elephants (Loxodonta africana) managed by combined protected and modified-protected contact and trained through operant conditioning. An initial hand-injection of detomidine hydrochloride and butorphanol tartrate at a ratio of 1:1 on a microg:microg basis was administered intramuscularly, with a dosage range of 50-70 mg (12.9-19.7 microg/kg) for each drug. The initial injection resulted in adequate sedation for initiation and completion of eight procedures, whereas supplemental doses were required for the remaining procedures. The dosage range for the supplemental injections of each drug was 4.0-7.3 microg/kg. Initial effect was noted within 3.0-25 min (mean = 11.6 min, SD +/- 5.9 min), with maximal effect occurring at 25-30 min for those procedures not requiring supplementation. In all but one procedure, this effect was maintained until the end of the procedure, which ranged from 47 to 98 min (mean = 74.7 min, SD +/- 18.8 min). No cardiac or respiratory depression was appreciated. Recovery after administration of reversal agents was rapid and complete, ranging from 2 to 20 min (mean = 9.0 min, SD +/- 7.0 min). On the basis of the authors' experience, recommended dosage ranges for reversal agents would be intravenous yohimbine (73.4-98.5 microg/kg), intravenous naltrexone (48.9-98.5 microg/kg), and intramuscular naltrexone (73.4-98.5 microg/kg). Approximately one-third to one-half of the total naltrexone dose should be administered intravenously. Mild adverse side effects limited to the gastrointestinal tract were observed in association with five procedures including abdominal distention with or without transient anorexia. Administration of reversal agents, encouraging exercise and water consumption, and administration of flunixin meglumine were helpful in the resolution of signs. In addition to gastrointestinal signs, slight ataxia was observed before initiation of surgical stimulation during one procedure in which 19.7 microg/kg of each drug was administered. On the basis of the procedures that did not require supplementation to initiate treatment and taking into consideration the potential for ataxia at higher doses, a starting dosage range of 14.7-16.2 microg/kg of both detomidine and butorphanol in a ratio of 1:1 on a microg:microg basis administered i.m. simultaneously is recommended.     

Cardiovascular effects of medetomidine, detomidine and xylazine in horses

The cardiovascular effects of medetomidine, detomidine, and xylazine in horses were studied. Fifteen horses, whose right carotid arteries had previously been surgically raised to a subcutaneous position during general anesthesia were used. Five horses each were given the following 8 treatments: an intravenous injection of 4 doses of medetomidine (3, 5, 7.5, and 10 microg/kg), 3 doses of detomidine (10, 20, and 40 microg/kg), and one dose of xylazine (1 mg/kg). Heart rate decreased, but not statistically significant. Atrio-ventricular block was observed following all treatments and prolonged with detomidine. Cardiac index (CI) and stroke volume (SV) were decreased with all treatments. The CI decreased to about 50% of baseline values for 5 min after 7.5 and 10 microg/kg medetomidine and 1 mg/kg xylazine, for 20 min after 20 microg/kg detomidine, and for 50 min after 40 microg/kg detomidine. All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. Hypertension was significantly prolonged in 20 and 40 microg/kg detomidine. The hypotensive phase was not observed in 10 microg/kg medetomidine or detomidine. The changes in ABP were associated with an increase in peripheral vascular resistance. Respiratory rate was decreased for 40 to 120 min in 5, 7.5, and 10 microg/kg medetomidine and detomidine. The partial pressure of arterial oxygen decreased significantly in 10 microg/kg medetomidine and detomidine, while the partial pressure of arterial carbon dioxide did not change significantly. Medetomidine induced dose-dependent cardiovascular depression similar to detomidine. The cardiovascular effects of medetomidine and xylazine were not as prolonged as that of detomidine. KEY WORDS: cardiovascular effect, detomidine, equine, medetomidine, xylazine.     

Investigation of romifidine and detomidine for the clinical sedation of horses

The effects of two intravenous doses of romifidine (80 and 120 microg/kg) and one dose of detomidine (20 microg/kg) were compared in a blinded study in 30 horses requiring to be sedated for routine dental treatment. Several physiological parameters were assessed before and for two hours after the administration of the drugs, and the horses' teeth were rasped 30 minutes after they were administered. Romifidine produced a dose-dependent effect on most parameters. Detomidine at 20 microg/kg was similar to romifidine at 120 microg/kg in the magnitude of its sedative effects, but was similar to romifidine at 80 pg/kg in its duration. There were no significant differences between the three treatments in terms of the clinical procedure score.     

Anti-nociceptive efficacy of carprofen, levomethadone and buprenorphine for pain relief in cats following major orthopaedic surgery

A placebo-controlled, randomized blind study was conducted in cats (n = 60) after fracture repair to compare the analgesic effects as well as the side-effects of carprofen, buprenorphine and levomethadone during a 5-day treatment. Cats with severe shock symptoms or increases in blood urea nitrogen (BUN) and creatinine were excluded from the study. The cats were randomly assigned to four groups (n= 15). In group 1, carprofen was administered upon extubation at an initial dose of 4 mg/kg body weight, followed by one-third of that dose three times daily on days 2 to 5. In group 2, buprenorphine was administered in a single dose of 0.01 mg/kg body weight upon extubation and subsequently every 8 h. Levomethadone (group 3) was applied according to the same scheme at a dosage of 0.3 mg/kg body weight each time. The placebo (group 4) was given at the same time intervals as the opioids. Examinations were carried out prior to anaesthesia, between 30 min and 8 h after extubation, and on the following 4 days, 1 h after administration of the analgesics or the placebo as well as 1 h before the next administration. Pain and sedation evaluation was carried out with a visual analogue system (VAS) and with the aid of a numerical estimation scale (NRS). Pain was also scored by measuring mechanical nociceptive threshold of traumatized tissue. Plasma glucose and cortisol concentration, heart rate, respiration rate, blood pressure and body temperature were measured. Furthermore, a complete blood count and clinical chemistry including BUN, creatinine, alanine aminotransferase (ALT), glutamate dehydrogenase (GLDH), arterial blood pressure (AP), total protein and electrolytes of the cats were checked on the day of admission as well as on the last day of this study (day 5). Defaecation and urination as well as wound healing were monitored. On the basis of the mechanical nociceptive threshold of the traumatized tissue, concentrations of plasma glucose and cortisol and pain assessment using NRS and VAS, carprofen was found to have better anti-nociceptive efficacy when compared with the two opioid analgesics, while the analgesic effect of levomethadone was similar to that of buprenorphine. However, the carprofen group also showed comparably high median NRS and VAS pain scores in addition to occasional broad deviations from the group mean on the first post-operative treatment day. Sedative effects were detected for buprenorphine and levomethadone; in addition, symptoms of central excitation were noted with levomethadone. There was no indication of any clinically relevant respiratory depressive or cardiovascular effects, nor of any undesired renal, gastrointestinal or hepatic effects of the analgesics applied. However, the somewhat insensitive examination methods did not permit sufficient evaluation of side-effects, particularly on the gastrointestinal tract and the kidneys. It was found that carprofen and buprenorphine were well-tolerated analgesics for a 5-day administration in the cat, whereas levomethadone caused central excitation in some cases in the dosage scheme used here. However, it was apparent that none of the tested analgesics induced sufficient analgesia in the post-operative phase. For this reason, suitable methods must be found to improve analgesia, particularly in the immediate post-operative phase.     

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.     

The Influence of Detomidine and Epinephrine on Heart Rate, Arterial Blood Pressure, and Cardiac Arrhythmia in Horses

Detomidine (10 micrograms/kg and 20 micrograms/kg) was administered to seven horses with and without epinephrine infusion (0.1 microgram/kg/min) from 5 minutes before to 5 minutes after detomidine injection. One or more single supraventricular premature heartbeats were observed in three horses after detomidine administration. Epinephrine infusion did not modify the incidence of cardiac arrhythmias in detomidine-treated horses at the doses tested. Relatively high momentary peak systolic pressures were registered in some horses after detomidine administration during epinephrine infusion. The highest systolic arterial blood pressure was 290 mm Hg, but this value was not higher than that reported in horses during maximum physical exercise. Epinephrine infusion did not alter blood gases, arterial pH, or base excess.     

Clinical effect of buprenorphine or butorphanol,in combination with detomidine and diazepam,on sedation and postoperative pain after cheek tooth extraction in horses

The objective of this study was to compare effects of butorphanol (BUT) or buprenorphine (BUP), in combination with detomidine and diazepam, on the sedation quality, surgical conditions, and postoperative pain control after cheek tooth extraction in horses, randomly allocated to 2 treatment groups (BUT: n = 20; BUP: n = 20). A bolus of detomidine (15 μg/kg, IV) was followed by either BUP (7.5 μg/kg, IV) or BUT (0.05 mg/kg, IV). After 20 min, diazepam (0.01 mg/kg, IV) was administered and sedation was maintained with a detomidine IV infusion (20 μg/kg/h), with rate adjusted based on scores to 5 variables. All horses received a nerve block (maxillary or mandibular), and gingival infiltration with mepivacaine. Sedation quality was assessed by the surgeon from 1 (excellent) to 10 (surgery not feasible). A pain scoring system (EQUUS-FAP) was used to assess postoperative pain. Serum cortisol concentrations and locomotor activity (pedometers) were measured.Horses in BUP and BUT required a median detomidine infusion rate of 30.2 μg/kg/h (20 to 74.4 μg/kg/h) and 32.2 μg/kg/h (20 to 48.1 μg/kg/h), respectively (P = 0.22). Horses in the BUP group had better sedation quality (P < 0.05) during surgery and higher step counts (P < 0.001) postoperatively. Buprenorphine combined with detomidine provided a more reliable sedation than butorphanol. However, the EQUUS-FAP pain scale became unreliable because of BUP-induced excitement behavior.     

Analgesic effect of butorphanol in ponies following castration

Reasons for performing study: In the UK butorphanol has a marketing authorisation for administration to horses for sedation in combination with detomidine, and at a higher dose (0.1 mg/kg bwt), for the alleviation of pain. There is only a limited number of clinical studies designed to examine the analgesic effects of butorphanol administration following surgery. Objective: To investigate the effect of premedication with butorphanol on post operative pain following castration under general anaesthesia in ponies. Hypothesis: Ponies receiving butorphanol would experience less pain after castration than ponies that did not receive butorphanol. Methods: A randomised, observer blinded clinical study in which 20 ponies received butorphanol and detomidine (Group B) or detomidine alone (Group C). Anaesthesia was induced with ketamine and diazepam and open castration performed. Pain was assessed by one individual using a dynamic interactive visual analogue scale (DIVAS) 100 mm in length (0 = no pain, 100 mm the maximum possible pain for that procedure). ‘Rescue’ analgesia was administered when DIVAS >50 mm and was butorphanol i.v. On the second occasion DIVAS was >50 mm, flunixin was administered i.v. Data from the DIVAS were analysed using a Mann Whitney Test. Results: Only one animal did not require rescue analgesia after surgery (Group C). DIVAS were not significantly different between groups (P = 0.063). Conclusions and potential relevance: Castration is sufficiently painful that administration of a single preoperative dose of butorphanol does not provide adequate post operative analgesia.     

Sedative effect of detomidine in infant calves.

Detomidine administered intramuscularly at a dose of 10, 20 or 40 micrograms/kg body mass was evaluated for its sedative effects in 15 unfasted infant calves (age: 15-20 days; body mass: 18-33 kg). The drug produced dose-dependent sedation. At a dose of 10 micrograms/kg detomidine produced effective sedation for 30 to 45 min without any observable analgesia. At doses of 20 or 40 micrograms/kg it caused deep sedation, sternal recumbency, and moderate analgesia of the trunk. Hyperglycaemia was recorded at all dose levels. The changes in respiratory rate, rectal temperature, haemoglobin, packed cell volume, total erythrocyte count and plasma concentration of total protein were not significant.     

Analgesic effects of butorphanol in horses: dose-response studies

The analgesic effects of butorphanol (0.05, 0.1, 0.2, and 0.4 mg/kg), pentazocine (2.2 mg/kg), and butorphanol vehicle (0.04 ml/kg) were observed in 6 horses. These horses were instrumented to measure response objectively to painful superficial and visceral stimuli. The tested drugs were given IV according to a Latin square design. After preinjection base-line measurements were made, the analgesic effects were observed at 15 and 30 minutes and then at 30-minute intervals until postinjection minute 240. Analgesic effects of butorphanol were dose-related, with durations between 15 and 90 minutes. Duration of analgesia after pentazocine (2.2 mg/kg) was given was between 15 and 30 minutes. When compared with pentazocine, the 0.4 mg/kg dose of butorphanol provided a more intense and longer period of analgesia. A butorphanol dose of 0.2 mg/kg IV appears optimal. On a dose-body weight basis, the potency of butorphanol was 10 to 17 times that of pentazocine. Behavioral side effects were noted with both agents and were dose-related.