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.     

Influence of detomidine and xylazine on spleen dimensions and on splenic response to epinephrine infusion in healthy adult horses

ObjectiveTo compare the changes in splenic length and thickness and in packed cell volume (PCV) following detomidine or xylazine administration and subsequent epinephrine infusion. Hypothesis: Spleen relaxation occurs following xylazine or detomidine administration and interferes with subsequent splenic contractile response to epinephrine.Study designRandomized non‐blinded crossover experimental study.Animals6 healthy adult mares.MethodsThe mares received an intravenous (IV) epinephrine infusion (1 μg kg^?1minute^?1 over 5 minutes) one hour after IV administration of detomidine (0.01 mg kg^?1), xylazine (0.5 mg kg^?1) or no drug (control), with a withdrawal period of at least 7 days between experiments. The splenic length measured in two different axes, the splenic thickness, and the PCV were measured prior to sedation (T0), 30 minutes later, and at 5‐minute intervals from the start of the epinephrine infusion (T1) until T1 + 40 minutes. Changes from base‐line and between treatments were compared using a two‐way anova for repeated measures. Significance was set at p < 0.05.ResultsSplenic length was significantly increased and PCV was significantly decreased after detomidine administration compared to baseline. Epinephrine infusion resulted in a significant decrease in splenic length and thickness, and a significant increase in PCV, irrespective of prior treatment with detomidine or xylazine.ConclusionsDetomidine administration was followed by a sonographically detectable increase of splenic length. Neither detomidine nor xylazine interfered with the ability of the spleen to contract following subsequent administration of an epinephrine infusion given one hour later.Clinical relevancePrevious sedation with alpha‐2 agonists does not preclude the efficiency of epinephrine as a medical treatment of left dorsal displacement of the large colon, but further investigations are required with other drug doses and different time intervals between administrations.     

Effects of alpha2-adrenergic receptor agonists on urine production in horses deprived of food and water

OBJECTIVE: To quantitate the dose- and time-related effects of IV administration of xylazine and detomidine on urine characteristics in horses deprived of feed and water. ANIMALS: 6 horses. PROCEDURE: Feed and water were withheld for 24 hours followed by i.v. administration of saline (0.9% NaCI) solution, xylazine (0.5 or 1.0 mg/kg), or detomidine (0.03 mg/kg). Horses were treated 4 times, each time with a different protocol. Following treatment, urine and blood samples were obtained at 15, 30, 60, 120, and 180 minutes. Blood samples were analyzed for PCV and serum concentrations of total plasma solids, sodium, and potassium. Urine samples were analyzed for pH and concentrations of glucose, proteins, sodium, and potassium. RESULTS: Baseline (before treatment) urine flow was 0.30 +/- 0.03 mL/kg/h and did not significantly change after treatment with saline solution and low-dose xylazine but transiently increased by 1 hour after treatment with high-dose xylazine or detomidine. Total urine output at 2 hours following treatment was 312 +/- 101 mL versus 4,845 +/- 272 mL for saline solution and detomidine, respectively. Absolute values of urine concentrations of sodium and potassium also variably increased following xylazine and detomidine administration. CONCLUSIONS AND CLINICAL RELEVANCE: Xylazine and detomidine administration in horses deprived of feed and water causes transient increases in urine volume and loss of sodium and potassium. Increase in urine flow is directly related to dose and type of alpha2-adrenergic receptor agonist. Dehydration in horses may be exacerbated by concurrent administration of alpha2-adrenergic receptor agonists.     

Cardiovascular effects of xylazine and detomidine in horses

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, IV; xylazine, 2.2 mg/kg, IM; detomidine, 0.01 mg/kg, IV; detomidine, 0.02 mg/kg, IV; and detomidine, 0.04 mg/kg, IM. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following IV administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, IV administration of 0.02 mg of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, +dP/dt and -dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The PCV was significantly reduced by all treatments. Respiratory rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 IV treatments only.     

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.     

Plasma biochemistry reference values of wild bonnethead sharks,Sphyrna tiburo

Background — Elasmobranchs (sharks, skates, and rays) are of commercial, sport, research, and exhibit importance, however, blood chemistry reference values have been determined for few of these species. Objectives — The purpose of this study was to establish plasma biochemistry and PCV reference values for wild bonnethead sharks (Sphyrna tiburo). Methods — Heparinized blood samples were collected from 24 bonnethead sharks at the time of capture in trawl nets off the coast of South Carolina and Georgia. Weight, length, PCV, total solids (TS, by refractometry), and plasma biochemical analyses were done using standard techniques. Wilcoxon rank‐sum and Kendall tau b tests were used to compare values by animal size, boat and sex; 1–way ANOVA was used to compare TS and total protein (TP) concentrations. Results — Median (quartiles; minimum‐maximum) values were as follows: PCV 22% (22%, 26%; 17–28%), TS 6.3 (6.0, 6.8; 5.8–7.5) g/dL, total protein 2.9 (2.7,3.4; 2.2–4.3) g/dL, albumin 0.4 (0.4,0.4; 0.3–0.5) g/dL, globulins 2.6 (2.3,3.0; 1.9–3.8) g/dL, sodium 282 (279, 285; 273–292) mmol/L, potassium 7.3 (6.4, 7.9; 5.7–9.2) mmol/L, chloride 290 (285, 296; 277–304) mmol/L, total CO₂ 3 (2, 4; 0–5) mmol/L, calcium 16.8 (16.2,17.4; 15.8–18.2) mg/dL, phosphorus 8.8 (7.5,10.0; 5.9–12.7) mg/dL, urea nitrogen 1004 (986, 1028; 944–1068) mg/dL, creatinine <0.1 mg/dL, glucose 184 (165, 191; 155–218) mg/dL, aspartate aminotransferase 42 (33, 66; 15–132) U/L, lactate dehydrogenase <5 U/L, creatine kinase 82 (47, 233; 18–725) U/L, and osmolality 1094 (1078,1111; 1056–1139) mOsm/kg. No differences based on sex were detected. TS and total TP values were related by the fitted line TS = (1.006 × TP) + 3.318. Conclusions — Values reported here will be useful for evaluating the health status of bonnetheads in wild and captive research conditions and in exhibits.     

Effects of Epinephrine,Detomidine, and Butorphanol on Assessments of Insulin Sensitivity in Mares

Sympathoadrenal stimulation may perturb results of endocrine tests performed on fractious horses. Sedation may be beneficial; however, perturbation of results may preclude useful information. Four experiments were designed to 1) determine the effects of epinephrine on insulin response to glucose (IR2G), 2) assess the effects of detomidine (DET), alone or combined with butorphanol (DET/BUT), on IR2G and glucose response to insulin (GR2I), and 3) assess the effects of BUT alone on IR2G. In Experiment 1, mares were administered saline or epinephrine (5 μg/kg BW) immediately before infusion of glucose (100 mg/kg BW). Glucose stimulated (P < .05) insulin release in controls at 5 minutes that persisted through 30 minutes; insulin was suppressed (P < .05) by epinephrine from 5 to 15 minutes, rising gradually through 30 minutes. Experiments 2 (IR2G) and 3 (GR2I) were conducted as triplicated 3 × 3 Latin squares with the following treatments: saline (SAL), DET, and DET/BUT (all administered at .01 mg/kg BW). Glucose stimulated (P < .05) insulin release that persisted through 30 minutes in SAL mares; DET and DET/BUT severely suppressed (P < .0001) the IR2G. Sedation did not affect resting glucose and had inconsistent effects on the GR2I when mares were treated with 50 mIU/kg BW recombinant human insulin. Butorphanol had no effect on IR2G. In conclusion, adrenergic agonists severely suppress the IR2G and cannot be used for sedation for this test. The use of DET did not alter the GR2I, and therefore may be useful for conducting this test in fractious horses.     

Detomidine reduces isoflurane anesthetic requirement (MAC) in horses

Objective To quantitate the dose‐ and time‐related magnitude of the anesthetic sparing effect of, and selected physiological responses to detomidine during isoflurane anesthesia in horses. Study design Randomized cross‐over study. Animals Three, healthy, young adult horses weighing 485 ± 14 kg. Methods Horses were anesthetized on two occasions to determine the minimum alveolar concentration (MAC) of isoflurane in O₂ and then to measure the anesthetic sparing effect (time‐related MAC reduction) following IV detomidine (0.03 and 0.06 mg kg^?1). Selected common measures of cardiopulmonary function, blood glucose and urinary output were also recorded. Results Isoflurane MAC was 1.44 ± 0.07% (mean ± SEM). This was reduced by 42.8 ± 5.4% and 44.8 ± 3.0% at 83 ± 23 and 125 ± 36 minutes, respectively, following 0.03 and 0.06 mg kg^?1, detomidine. The MAC reduction was detomidine dose‐ and time‐dependent. There was a tendency for mild cardiovascular and respiratory depression, especially following the higher detomidine dose. Detomidine increased both blood glucose and urine flow; the magnitude of these changes was time‐ and dose‐dependent Conclusions Detomidine reduces anesthetic requirement for isoflurane and increases blood glucose concentration and urine flow in horses. These changes were dose‐ and time‐related. Clinical relevance The results imply potent anesthetic sparing actions by detomidine. The detomidine‐related increased urine flow should be considered in designing anesthetic protocols for individual horses.     

Stress responses during total intravenous anaesthesia in ponies with detomidine - guaiphenesin - ketamine

Six ponies were anaesthetised for two hours with intermittent injections of a combination of guaiphenesin (72 mg/kg/hr), ketamine (1.4 mg/kg/hr) and detomidine (0.015 mg/kg/hr) after premedication with detomidine 0.01 mg/kg and induction of anaesthesia with guaiphenesin 50 mg/kg and ketamine 2 mg/kg. Induction of anaesthesia was smooth, the ponies were easily intubated and after intubation breathed 100% oxygen spontaneously. During anaesthesia mean pulse rate ranged between 31–44 beats per minute and mean respiratory rate between 12–23 breaths per minute. Mean arterial blood pressure remained between 110–130 mm Hg, mean arterial carbon dioxide tension between 6.1–6.9 kPa and pH between 737–7.42. Arterial oxygen tension was over 23 kPa throughout anaesthesia. Plasma glucose increased to more than 25 mmol per litre during anaesthesia; there was no change in lactate or ACTH concentration and plasma cortisol concentration decreased. Recovery was rapid and smooth. A guaiphenesin, ketamine and detomidine combination appeared to offer potential as a total intravenous technique for maintenance of anaesthesia in horses.     

Effects of Intravenous Detomidine on Schirmer Tear Test Results in Clinically Normal Horses

This study was conducted to determine the effects of intravenous detomidine on Schirmer tear test (STT) results in clinically normal horses. Eighteen adult horses were randomly divided into two groups of nine horses each. The treatment group was sedated with intravenous detomidine alone (20 μg/kg), and the control group received only intravenous saline (0.2 mL/100 kg). Schirmer tear test was performed just before intravenous administration of detomidine or saline in treatment and control groups, respectively. Schirmer tear tests were repeated 5, 20, 60, and 120 minutes later. Horses enrolled in this study consisted of nine males and nine females. Breeds were Arabian and Hanoverian, ranging from 3 to 6 years in age. In the treatment group, the pretreatment and subsequent posttreatment mean ± standard deviation values were 17.0 ± 6.9 (0 minutes), 11.8 ± 2.9 (5 minutes), 12.1 ± 2.0 (20 minutes), 12.1 ± 3.1 (60 minutes), and 15.0 ± 2.8 (120 minutes) mm wetting/min. In this group of horses, a significant reduction was observed in STT values at 5, 20, and 60 minutes after treatment with detomidine hydrochloride in comparison to the pretreatment values (analysis of variance with post hoc testing; P₅ = 0.004, P₂₀ = 0.007, P₆₀ = 0.006). There was no significant difference between baseline values and posttreatment values in the control saline group (P ≥ .08). We conclude that intravenous detomidine causes a significant reduction in STT values in clinically normal horses. In horses, practitioners should measure STT values before intravenous administration of detomidine to accurately assess the results.     

Propofol compared with propofoVguaiphenesin after detornidine premedication for equine surgery

Anaesthesia using propofol alone and in combination with guaiphenesin, after detomidine premedication, was evaluated for performance of minor surgical procedures (castration and tenotomy) in horses. Twelve male horses were premedicated with 0.015 mg/kg of detomidine intravenously (iv) and divided into two groups of six. One group of horses received 2 mg/kg of propofol iv and the other group received 0.5 mg/kg of propofol mixed with 100 mg/kg of a 7.5% solution of guaiphenesin in saline iv. Induction of anaesthesia was fast and smooth in both groups. All horses were easily intubated immediately afterwards but intubation was easier in the horses which received propofol and guaiphenesin. Heart rate fell by 20% in both groups after detomidine injection, stabilising between 45 and 53 beats/minute during anaesthesia with no difference between the groups. Respiratory depression developed after detomidine injection and was slightly intensified after induction of anaesthesia. Respiratory rate was significantly lower in the propofol group (14 ± 3 breaths/minute) than with propofol/guaiphenesin (19 ± 4 breaths/minute) at five minutes after induction. Anaesthesia induced respiratory acidosis in both groups and hypoxaemia also occurred, but once the horses stood up the arterial blood oxygen partial pressure returned to basal values. Surgical time ranged between 8 and 16 minutes and with the exception of one horse in the propofol/guaiphenesin group the horses did not show signs of pain or discomfort during surgery. Recovery to standing was fast and took 26 ± 2 minutes in the propofol and 29 ± 5 minutes in the propofol/ guaiphenesin group. Most horses stood up at the first attempt with minimal ataxia. These two anaesthetic techniques appear to be useful for minor surgical procedures performed within 16 minutes of induction of anaesthesia.     

Effects of anesthetic protocols on electroejaculation variables of Iberian ibex (Capra pyrenaica)

The effects of three intramuscular anesthesia protocols - detomidine 190 μg/kg plus ketamine 2 mg/kg, detomidine 270 μg/kg plus ketamine 1.4 mg/kg, and tiletamine 3.4 mg/kg plus zolazepam 3.4 mg/kg - on penis protrusion and ejaculation variables were compared in nine captive Spanish ibex (Capra pyrenaica) subjected to electroejaculation. Body temperature, heart, and respiratory rates, as well as a number of plasma biochemical variables were also recorded prior to and during anesthesia. The detomidine plus ketamine protocols induced bradycardia and increased respiratory rate. However, the tiletamine/zolazepam protocol did not affect heart and respiratory rates. None of the three protocols caused a substantial change in rectal temperature, yet all protocols caused a significant increase in plasma glucose levels. Differences in anesthetic protocols did not affect sperm quality or quantity. However, choice of anesthetic protocol affected (P < 0.05) the degree of penis protrusion and the electrical pulse sequence required to achieve ejaculation. Results of this study support a recommendation of detomidine 270 μg/kg plus ketamine 1.4 mg/kg for anesthesia of Spanish ibex undergoing electroejaculation.     

Effects of anesthesia, surgery, and intravenous administration of fluids on plasma antidiuretic hormone concentrations in healthy dogs

OBJECTIVE: To evaluate effects of anesthesia, surgery, and intravenous administration of fluids on plasma concentrations of antidiuretic hormone (ADH), concentration of total solids (TS), PCV, arterial blood pressure (BP), plasma osmolality, and urine output in healthy dogs. ANIMALS: 22 healthy Beagles. PROCEDURE: 11 dogs did not receive fluids, and 11 received 20 ml of lactated Ringer's solution/kg of body weight/h. Plasma ADH adn TS concentrations, PCV, osmolality, and arterial BP were measured before anesthesia (T0) and after administration of preanesthetic agents (T1), induction of anesthesia (T2), and 1 and 2 hours of surgery (T3 and T4, respectively). Urine output was measured at T3 and T4. RESULTS: ADH concentrations increased at T1, T3, and T4, compared with concentrations at T0. Concentration of TS and PCV decreased at all times after administration of preanesthetic drugs. Plasma ADH concentration was less at T3 in dogs that received fluids, compared with those that did not. Blood pressure did not differ between groups, and osmolality did not increase > 1% from To value at any time. At T4, rate of urine production was less in dogs that did not receive fluids, compared with those that did. CONCLUSIONS AND CLINICAL RELEVANCE: Plasma ADH concentration increased and PCV and TS concentration decreased in response to anesthesia and surgery. Intravenous administration of fluids resulted in increased urine output but had no effect on ADH concentration or arterial BP. The causes and effects of increased plasma ADH concentrations may affect efficacious administration of fluids during the perioperative period in dogs.     

Cardiorespiratory and metabolic effects of xylazine, detomidine, and a combination of xylazine and acepromazine administered after exercise in horses

OBJECTIVE: To determine sedative, cardiorespiratory and metabolic effects of xylazine hydrochloride, detomidine hydrochloride, and a combination of xylazine and acepromazine administered i.v. at twice the standard doses in Thoroughbred horses recuperating from a brief period of maximal exercise. ANIMALS: 6 adult Thoroughbreds. PROCEDURE: Horses were preconditioned by exercising them on a treadmill to establish a uniform level of fitness. Each horse ran 4 simulated races, with a minimum of 14 days between races. Simulated races were run at a treadmill speed that caused horses to exercise at 120% of their maximal oxygen consumption. Horses ran until they were fatigued or for a maximum of 2 minutes. One minute after the end of exercise, horses were treated i.v. with xylazine (2.2 mg/kg of body weight), detomidine (0.04 mg/kg), a combination of xylazine (2.2 mg/kg) and acepromazine (0.04 mg/kg), or saline (0.9% NaCl) solution. Treatments were randomized so that each horse received each treatment once, in random order. Cardiopulmonary indices were measured, and samples of arterial and venous blood were collected immediately before and at specific times for 90 minutes after the end of each race. RESULTS: All sedatives produced effective sedation. The cardiopulmonary depression that was induced was qualitatively similar to that induced by administration of these sedatives to resting horses and was not severe. Sedative administration after exercise prolonged the exercise-induced increase in body temperature. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of xylazine, detomidine, or a combination of xylazine-acepromazine at twice the standard doses produced safe and effective sedation in horses that had just undergone a brief, intense bout of exercise.     

Comparison of detomidine and romifidine as premedicants before ketamine and halothane anesthesia in horses undergoing elective surgery

OBJECTIVE: To compare detomidine hydrochloride and romifidine as premedicants in horses undergoing elective surgery. ANIMALS: 100 client-owned horses. PROCEDURE: After administration of acepromazine (0.03 mg/kg, IV), 50 horses received detomidine hydrochloride (0.02 mg/kg of body weight, IV) and 50 received romifidine (0.1 mg/kg, IV) before induction and maintenance of anesthesia with ketamine hydrochloride (2 mg/kg) and halothane, respectively. Arterial blood pressure and blood gases, ECG, and heart and respiratory rates were recorded. Induction and recovery were timed and graded. RESULTS: Mean (+/- SD) duration of anesthesia for all horses was 104 +/- 28 minutes. Significant differences in induction and recovery times or grades were not detected between groups. Mean arterial blood pressure (MABP) decreased in both groups 30 minutes after induction, compared with values at 10 minutes. From 40 to 70 minutes after induction, MABP was significantly higher in detomidine-treated horses, compared with romifidine-treated horses, although more romifidine-treated horses received dobutamine infusions. In all horses, mean respiratory rate ranged from 9 to 11 breaths/min, PaO2 from 200 to 300 mm Hg, PaCO2 from 59 to 67 mm Hg, arterial pH from 7.33 to 7.29, and heart rate from 30 to 33 beats/min, with no significant differences between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine and romifidine were both satisfactory premedicants. Romifidine led to more severe hypotension than detomidine, despite administration of dobutamine to more romifidine-treated horses. Both detomidine and romifidine are acceptable alpha2-adrenoceptor agonists for use as premedicants before general anesthesia in horses; however, detomidine may be preferable when maintenance of blood pressure is particularly important.     

Comparison of detomidine hydrochloride, xylazine, and xylazine plus morphine in horses: a double blind study

Detomidine (30 mcg/kg), xylazine (1.1 mg/kg) and xylazine/morphine (1.1 mg/kg and 0.75 mg/kg with 300 mg maximum dose) were compared in horses admitted for broncho-alveolar lavage. Horses (n=99) were randomized and clinicians performing the procedure were unaware of the sedation used. Horses were assessed during the procedure and for the next 2 hours. A significant number of xylazine/morphine-sedated horses showed excitement (p<0.05). The frequency of sinus block or arrest and second-degree atrioventricular block was significantly greater with detomidine. Detomidine-sedated horses were significantly more depressed than either xylazine or xylazine/morphine treated animals. Heart rate was significantly greater in horses given xylazine/morphine by 60 min. There was no significant difference between drug treatments related to reactions to the procedure or respiratory rate depression. The study indicated that all three methods are suitable for standing restraint. The more frequent adverse side effects (circling, muscle fasciculations, head pressing) accompanying xylazine/morphine should be considered.     

Effects of three antagonists on selected pharmacodynamic effects of sublingually administered detomidine in the horse

ObjectiveTo describe the effects of alpha₂-adrenergic receptor antagonists on the pharmacodynamics of sublingual (SL) detomidine in the horse.Study designRandomized crossover design.AnimalsNine healthy adult horses with an average age of 7.6 ± 6.5 years.MethodsFour treatment groups were studied: 1) 0.04 mg kg^?1 detomidine SL; 2) 0.04 mg kg^?1 detomidine SL followed 1 hour later by 0.075 mg kg^?1 yohimbine intravenously (IV); 3) 0.04 mg kg^?1 detomidine SL followed 1 hour later by 4 mg kg^?1 tolazoline IV; and 4) 0.04 mg kg^?1 detomidine SL followed 1 hour later by 0.12 mg kg^?1 atipamezole IV. Each horse received all treatments with a minimum of 1 week between treatments. Blood samples were obtained and plasma analyzed for yohimbine, atipamezole and tolazoline concentrations by liquid chromatography-mass spectrometry. Behavioral effects, heart rate and rhythm, glucose, packed cell volume (PCV) and plasma proteins were monitored.ResultsChin-to-ground distance increased following administration of the antagonists, however, this effect was transient, with a return to pre-reversal values as early as 1 hour. Detomidine induced bradycardia and increased incidence of atrioventricular blocks were either transiently or incompletely antagonized by all antagonists. PCV and glucose concentrations increased with tolazoline administration, and atipamezole subjectively increased urination frequency but not volume.Conclusions and clinical relevanceAt the doses administered in this study, the alpha₂-adrenergic antagonistic effects of tolazoline, yohimbine and atipamezole on cardiac and behavioral effects elicited by SL administration of detomidine are transient and incomplete.     

The effects of xylazine,detomidine, acepromazine and butorphanol on equine solid phase gastric emptying rate

The aim of this study was to measure the effects of specific commonly used sedative protocols on equine solid phase gastric emptying rate, using the 13C-octanoic acid breath test (13C-OABT). The gastric emptying of a standard 13C-labelled test meal was measured once weekly in 8 mature horses over two 4 week treatment periods. Each horse acted as its own control. In treatment Period 1, saline (2 ml i.v.), xylazine (0.5 mg/kg i.v.), detomidine (0.01 mg/kg i.v.) or detomidine/butorphanol combination (0.01/0.02 mg/kg i.v.) was administered in randomised order after ingestion of the test meal. During treatment Period 2, test meal consumption was followed by saline, xylazine (1.0 mg/kg i.v.), or detomidine (0.03 mg/kg i.v.) administration, or preceded by acepromazine (0.05 mg/kg i.m.) in randomised order. The 13C:12C ratio of sequential expiratory breath samples was determined by isotope ratio mass spectrometry, and used to measure the gastric half-emptying time, t 1/2, and duration of the lag phase, t lag, for each of the 64 tests. In treatment Period 1, detomidine/butorphanol prolonged both t 1/2 and t lag with respect to xylazine 0.5 mg/kg and the saline control (P < 0.05). In Period 2, detomidine 0.03 mg/kg delayed each parameter with respect to saline, acepromazine and xylazine 1.0 mg/kg (P < 0.001). Xylazine 1.0 mg/kg also lengthened t lag relative to the saline control (P = 0.0004), but did not cause a significant change in t 1/2. Comparison of treatment periods showed that the inhibitory effect of detomidine on gastric emptying rate was dose related (P<0.05). These findings may have clinical significance for case selection when these agents are used for purposes of sedation and/or analgesia.     

Efficacy of an Epidural Combination of Morphine and Detomidine in Alleviating Experimentally Induced Hindlimb Lameness in Horses

Amphotericin B-induced synovitis of the left tarsocrural joint was used to create a grade 3 of 4 lameness in 11 horses. Caudal epidural catheters were placed and advanced to the lumbosacral region. Baseline heart and respiratory rates were recorded and horses were videotaped at a walk and trot. Morphine sulphate (0.2 mg/kg) and detomidine hydrochloride (30 μg/kg) were administered to treated horses (n = 8) through the epidural catheter; an equivalent volume of physiologic saline solution was administered to control horses (n = 3) through the catheter. At hourly intervals after epidural injection for a total of 6 hours, heart and respiratory rates were recorded, and horses were videotaped walking and trotting. At the end of the observation period, video recordings were scrambled onto a master videotape. Lamenesses were scored by three investigators unaware of group assignment or treatment time. Lameness scores, heart rates, and respiratory rates were compared between groups using repeated measures analysis of variance. There was a significant decrease in lameness score after treatment with epidural morphine and detomidine ( P =.0003); average lameness scores of treated horses were less than grade 1 at each hourly observation for 6 hours after drug administration. Early in the observation period, heart rates significantly increased in control horses and decreased in treated horses ( P =.03). A similar trend occurred for respiratory rates ( P =.07). Results of this study demonstrate that epidural administration of a combination of morphine and detomidine is capable of providing profound hindlimb analgesia in horses.