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.     

Analgesic effect of butorphanol and levomethadone in detomidine sedated horses

The analgesic potency of butorphanol 25 microg/kg bodyweight (BW) and levomethadone 100 microg/kg BW, administered together with detomidine 10 microg/kg BW, was measured in twelve Warmblood horses in a randomized, blinded cross-over study. Detomidine with saline 10 ml 0.9% was used as placebo. The nociceptive threshold was determined using a constant current and a pneumatic pressure model for somatic pair Detomidine alone and in combination with butorphanol or levomethadone caused a significant temporary increase (P < 0.05) of the nociceptive threshold with a maximum effect within 15 min and a return to baseline levels within 90 min. Butorphanol and levomethadone increased the nociceptive threshold and prolonged the duration of anti-nociception significantly from 15 to 75 min (P < 0.05) after drug administration compared with detomidine alone to both test methods. No significant difference between butorphanol and levomethadone was registered. It is concluded that the addition of butorphanol or levomethadone to detomidine increases the nociceptive threshold to somatic pain and prolongs the analgesic effect of detomidine in the horse.     

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.     

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.     

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.     

Cardiopulmonary assessment of medetomidine, ketamine, and butorphanol anesthesia in captive Thomson's gazelles (Gazella thomsoni).

This investigation evaluated the cardiopulmonary effects of medetomidine, ketamine, and butorphanol anesthesia in captive juvenile Thomson's gazelles (Gazella thomsoni). Butorphanol was incorporated to reduce the dose of medetomidine necessary for immobilization and minimize medetomidine-induced adverse cardiovascular side effects. Medetomidine 40.1 +/- 3.6 microg/kg, ketamine 4.9 +/- 0.6 mg/kg, and butorphanol 0.40 +/- 0.04 mg/kg were administered intramuscularly by hand injection to nine gazelles. Times to initial effect and recumbency were within 8 min postinjection. Cardiopulmonary status was monitored every 5 min by measuring heart rate, respiratory rate, indirect blood pressure, end-tidal CO2, and indirect oxygen-hemoglobin saturation by pulse oximetry. Venous blood gases were collected every 15 min postinjection. Oxygen saturations less than 90% in three gazelles suggested hypoxemia. Subsequent immobilized gazelles were supplemented with intranasal oxygen throughout the anesthetic period. Sustained bradycardia (<60 beats per minute, as compared with anesthetized domestic calves, sheep, and goats) was noted in eight of nine gazelles. Heart and respiratory rates and rectal temperatures decreased slightly, whereas systolic, mean, and diastolic blood pressure values were consistent over the anesthetic period. Mild elevations in end tidal CO2 and PCO2 suggested hypoventilation. Local lidocaine blocks were necessary to perform castrations in all seven of the gazelles undergoing the procedure. Return to sternal recumbency occurred within 7 min and return to standing occurred within 12 min after reversal with atipamezole (0.2 +/- 0.03 mg/kg) and naloxone (0.02 +/- 0.001 mg/kg). Medetomidine, ketamine, and butorphanol can be used to safely anesthetize Thomson's gazelles for routine, noninvasive procedures. More invasive procedures, such as castration, can be readily performed with the additional use of local anesthetics.     

Reversible anesthesia of captive California sea lions (Zalophus californianus) with medetomidine, midazolam, butorphanol, and isoflurane.

Two adult California sea lions (Zalophus californianus) were effectively anesthetized 13 times with medetomidine (0.010-0.013 mg/kg), midazolam (0.2-0.26 mg/kg), and butorphanol (0.2-0.4 mg/kg) by i.m. hand or pole syringe injection. For each anesthetic event, atropine (0.02 mg/kg, i.m.) was administered 6-20 min after initial injections, and oxygen administration via face mask or nasal insufflation began at the same time. Light anesthesia was induced in 8-22 min and lasted 13-78 min. During eight of the procedures, isoflurane (0.5-2.0%) was administered via face mask or endotracheal tube for an additional 30-120 min to facilitate longer procedures or surgery. Anesthesia was antagonized with atipamezole (0.05-0.06 mg/kg) and naltrexone (0.1 mg/kg) in seven events, with the addition of flumazenil (0.0002-0.002 mg/kg) in six events. The antagonists were administered by i.m. injection 42-149 min after administration of the induction agents. All sea lions recovered to mild sedation within 4-17 min after administration of the antagonists.     

Duration of nonresponse to noxious stimulation after intramuscular administration of butorphanol, medetomidine, or a butorphanol-medetomidine combination during isoflurane administration in dogs

OBJECTIVE: To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO). ANIMALS: 6 healthy dogs. PROCEDURE: Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 microg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 microg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, end-tidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected. RESULTS: Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean +/- SD) was 0.0+/-0.0, 1.5+/-1.5, 2.63+/-0.49, and 5.58+/-2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone. CONCLUSION AND CLINICAL RELEVANCE: During ISO-induced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone.     

Comparison of etorphine-detomidine and medetomidine-ketamine anesthesia in captive addax (Addax nasomaculatus).

Thirty-five anesthetic events involving 15 captive addax (Addax nasonzaculatus) were performed between August 1998 and February 2002 using a combination of etorphine (33.7 +/- 7.9 microg/kg) and detomidine (21.9 +/- 4.6 microg/ kg) or a combination of medetomidine (57.4 +/- 8.6 microg/kg) and ketamine (1.22 +/- 0.3 microg/kg), with or without supplemental injectable or inhalant anesthetic agents. Etorphine-detomidine anesthesia was antagonized with diprenorphine (107.1 +/- 16.4 microg/kg) and atipamezole (100.9 +/- 42.4 microg/kg). Medetomidine-ketamine anesthesia was antagonized with atipamezole (245.3 +/- 63.4 microg/kg). Animals became recumbent within 5 min when the combination of etorphine and detomidine was used and within 11 min when the combination of medetomidine and ketamine was used. Both drug combinations were suitable for use as primary immobilizing agents producing short-duration restraint and analgesia. Bradycardia was noted with both combinations. Further investigation of the cardiopulmonary effects of both combinations is warranted.     

Carfentanil citrate used as an oral anesthetic agent for brown bears (Ursus arctos).

Carfentanil citrate was given orally to five adult brown bears (Ursus arctos) on 14 separate occasions during the winter and summer to determine effective anesthetic dosages and how season may alter these dosages. Lower blood urea nitrogen:creatinine ratios, depressed appetite, and decreased activity levels in the winter versus summer were reflective of different metabolic states, even though bears were not hibernating in the winter. Doses of carfentanil citrate between 6.0 and 15.2 microg/kg were mixed with 5-10 ml of honey, which the bears licked voluntarily from a spoon. During each anesthetization, respiratory and heart rates, hemoglobin saturation, temperature, electrocardiogram, blood gas values, and level of consciousness were monitored and utilized to determine effective dosages. Mean (+/- SE) dose requirements in the winter were 7.6 +/- 0.4 microg/kg, whereas a greater mean dose of 12.7 +/- 0.5 microg/kg was required in the summer (P < 0.05). After ingestion began, sternal recumbency occurred in an average of 7.5 min (range: 4-11 min), and full restraint and safe handling was achieved in 21 min (range: 8-40 min). At the end of each procedure, naltrexone was given as the reversal agent at a ratio of 100 mg naltrexone per 1 mg carfentanil, with 25% of the dose given i.v. or i.m. and 75% given s.c. Mean reversal time was 6 min after injection of naltrexone (range: 4-9 min). Rapid induction and recovery times and ease of oral administration make carfentanil citrate an effective anesthetic agent for use in brown bears. However, hypoventilation and respiratory acidosis were noted in all bears, and oxygen insufflation is recommended.     

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.     

Atipamezole in the management of detomidine overdose in a pony

OBSERVATIONS: A pony undergoing elective castration accidentally received an overdose of IV detomidine (200 microg kg(-1)) before anaesthesia was induced with ketamine and midazolam. A further 100 microg kg(-1) IV dose of detomidine was administered during anaesthesia. The mistake was recognized only when the animal failed to recover from anaesthesia in the expected time. The overdose (300 microg kg(-1) in total) was treated successfully with atipamezole, initially given IV and subsequently IM and titrated to effect to a total dose of 1100 microg kg(-1). The pony regained the standing position. A further injection of atipamezole (76 microg kg(-1) IM) was given 5 hours later to counteract slight signs of re-sedation. CONCLUSIONS: Atipamezole proved an effective antagonist for detomidine in a pony at an initial dose 3.65 x and a final total dose 3.9 x greater than the alpha2 agonist.     

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.     

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).     

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.     

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.     

Reversal of Oxymorphone Sedation by Naloxone, Nalmefene, and Butorphanol

The effects of naloxone (0.4 mg and 1.2 mg intravenously [IV]), nalmefene (0.03 mg/kg IV) and butorphanol (0.2 mg/kg IV and 0.4 mg/kg IV) on oxymorphone-induced sedation were studied in six dogs over a 4-hour observation period. The same dogs were observed for 4 hours untreated (unsedated control) and with oxymorphone sedation followed by saline solution (sedated control). The reversal drug or saline placebo was administered IV 20 minutes after oxymorphone (4.5 mg IV). Blinded observers evaluated the dogs for positional and attitudinal responses, heart rate, and respiratory rate. Sedated dogs treated with nalmefene most closely resembled unsedated dogs in all observed variables. Naloxone was most effective when administered at the higher dose. Mild renarcotization occurred in two dogs at hour 2, even after the higher naloxone dose. Residual sedation was observed in all dogs treated with 0.4 mg naloxone. Butorphanol resulted in partial reversal of sedation at both dosage levels. However, the degree of sedation was significantly less than that observed in the saline-treated controls, and it appeared that 0.4 mg/kg butorphanol may be clinically useful for opiate reversal in some situations.     

Comparison of two combinations of sedatives before anaesthetising pigs with halothane and nitrous oxide

Two groups of 21 three-month-old Landrace x Large White pigs were sedated with either azaperone (2 mg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group A), or detomidine (100 microg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group D) administered intramuscularly, before being anaesthetised with halothane, oxygen and nitrous oxide for a bilateral stifle arthrotomy. The pigs' heart rate, respiratory rate, mean arterial blood pressure, electrocardiogram, arterial oxygen saturation, arterial blood gases, and oesophageal and rectal temperature were measured while they were anaesthetised and five minutes after they were disconnected, and their recovery times and any complications were recorded. Both groups were well sedated. Their heart rate was unchanged during the period of anaesthesia but increased when they recovered. The respiratory rate, mean arterial blood pressure and rectal temperature were lower in group A than in group D (P<0.05). Mild respiratory acidosis developed during anaesthesia in both groups. Both groups recovered equally rapidly and complications were generally minor, though two pigs in group D appeared to develop malignant hyperthermia.     

The intravenous pharmacokinetics of butorphanol and detomidine dosed in combination compared with individual dose administrations to exercised horses

In equine and racing practice, detomidine and butorphanol are commonly used in combination for their sedative properties. The aim of the study was to produce detection times to better inform European veterinary surgeons, so that both drugs can be used appropriately under regulatory rules. Three independent groups of 7, 8 and 6 horses, respectively, were given either a single intravenous administration of butorphanol (100 µg/kg), a single intravenous administration of detomidine (10 µg/kg) or a combination of both at 25 (butorphanol) and 10 (detomidine) µg/kg. Plasma and urine concentrations of butorphanol, detomidine and 3-hydroxydetomidine at predetermined time points were measured by liquid chromatography–tandem mass spectrometry (LC-MS/MS). The intravenous pharmacokinetics of butorphanol dosed individually compared with co-administration with detomidine had approximately a twofold larger clearance (646 ± 137 vs. 380 ± 86 ml hr⁻¹ kg⁻¹) but similar terminal half-life (5.21 ± 1.56 vs. 5.43 ± 0.44 hr). Pseudo-steady-state urine to plasma butorphanol concentration ratios were 730 and 560, respectively. The intravenous pharmacokinetics of detomidine dosed as a single administration compared with co-administration with butorphanol had similar clearance (3,278 ± 1,412 vs. 2,519 ± 630 ml hr⁻¹ kg⁻¹) but a slightly shorter terminal half-life (0.57 ± 0.06 vs. 0.70 ± 0.11 hr). Pseudo-steady-state urine to plasma detomidine concentration ratios are 4 and 8, respectively. The 3-hydroxy metabolite of detomidine was detected for at least 35 hr in urine from both the single and co-administrations. Detection times of 72 and 48 hr are recommended for the control of butorphanol and detomidine, respectively, in horseracing and equestrian competitions.