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.     

In vitro effects of oxytocin,acepromazine, detomidine,xylazine, butorphanol,terbutaline, isoproterenol,and dantrolene on smooth and skeletal muscles of the equine esophagus

OBJECTIVE: To characterize the in vitro effects of oxytocin, acepromazine, xylazine, butorphanol, detomidine, dantrolene, isoproterenol, and terbutaline on skeletal and smooth muscle from the equine esophagus. ANIMALS: 14 adult horses without digestive tract disease. PROCEDURE: Circular and longitudinal strips from the skeletal and smooth muscle of the esophagus were suspended in tissue baths, connected to force-displacement transducers interfaced with a physiograph, and electrical field stimulation was applied. Cumulative concentration-response curves were generated for oxytocin, acepromazine, xylazine, detomidine, butorphanol, isoproterenol, terbutaline, and dantrolene. Mean maximum twitch amplitude for 3 contractions/min was recorded and compared with predrug-vehicle values for the skeletal muscle segments, and area under the curve (AUC) for 3 contractions/min was compared with predrug-vehicle values for the smooth muscle segments. RESULTS: No drugs caused a significant change in skeletal muscle response. In smooth muscle, isoproterenol, terbutaline, and oxytocin significantly reduced AUC in a concentration-dependent manner. Maximum reduction in AUC was 69% at 10(-4) M for isoproterenol, 63% at 10(-6) M for terbutaline, and 64% at 10(-4) M for oxytocin. CONCLUSIONS AND CLINICAL RELEVANCE: Isoproterenol, terbutaline, and oxytocin cause relaxation of the smooth muscle portion of the esophagus. The clinical relaxant effects on the proximal portion of the esophagus reported of drugs such as oxytocin, detomidine, and acepromazine may be the result of centrally mediated mechanisms.     

Intravenous anesthesia

Anticholinergics, tranquilizers, and sedative-hypnotics are the usual agents used for preanesthetic sedation of the horse. Of these drugs, the anticholinergics are of little importance in the horse. Acepromazine is the most useful and widely used tranquilizer, whereas xylazine is a safe and popular sedative. A newer sedative recently made available to the veterinarian for clinical use in horses is detomidine. Thiobarbiturates are seldom used alone any longer but are still useful when combined with guaifenesin for induction and maintenance of anesthesia. Other, more contemporary drug combinations that have largely replaced thiobarbiturates and chloral hydrate include xylazine with ketamine, xylazine with Telazol, detomidine with Telazol, and guaifenesin with ketamine and xylazine.     

Comparison of the effects of the alpha-2 agonists detomidine, romifidine and xylazine on nociceptive withdrawal reflex and temporal summation in horses

ObjectiveTo evaluate and compare the antinociceptive effects of the three alpha-2 agonists, detomidine, romifidine and xylazine at doses considered equipotent for sedation, using the nociceptive withdrawal reflex (NWR) and temporal summation model in standing horses.Study designProspective, blinded, randomized cross-over study.AnimalsTen healthy adult horses weighing 527–645 kg and aged 11–21 years old.MethodsElectrical stimulation was applied to the digital nerves to evoke NWR and temporal summation in the left thoracic limb and pelvic limb of each horse. Electromyographic reflex activity was recorded from the common digital extensor and the cranial tibial muscles. After baseline measurements a single bolus dose of detomidine, 0.02 mg kg^?1, romifidine 0.08 mg kg^?1, or xylazine, 1 mg kg^?1, was administered intravenously (IV). Determinations of NWR and temporal summation thresholds were repeated at 10, 20, 30, 40, 60, 70, 90, 100, 120 and 130 minutes after test-drug administration alternating the thoracic limb and the pelvic limb. Depth of sedation was assessed before measurements at each time point. Behavioural reaction was observed and recorded following each stimulation.ResultsThe administration of detomidine, romifidine and xylazine significantly increased the current intensities necessary to evoke NWR and temporal summation in thoracic limbs and pelvic limbs of all horses compared with baseline. Xylazine increased NWR thresholds over baseline values for 60 minutes, while detomidine and romifidine increased NWR thresholds over baseline for 100 and 120 minutes, respectively. Temporal summation thresholds were significantly increased for 40, 70 and 130 minutes after xylazine, detomidine and romifidine, respectively.Conclusions and clinical relevanceDetomidine, romifidine and xylazine, administered IV at doses considered equipotent for sedation, significantly increased NWR and temporal summation thresholds, used as a measure of antinociceptive activity. The extent of maximal increase of NWR and temporal summation thresholds was comparable, while the duration of action was drug-specific.     

Qualitative and quantitative characteristics of the electroencephalogram in normal horses after sedation

Background

The administration of certain sedatives has been shown to promote sleep in humans. Related agents induce sleep‐like behavior when administered to horses. Interpretation of electroencephalograms (EEGs) obtained from sedated horses should take into account background activity, presence of sleep‐related EEG events, and the animal's behavior.

Hypothesis

Sedatives induce states of vigilance that are indistinguishable on EEGs from those that occur naturally.

Animals

Six healthy horses.

Methods

Digital EEG with video was recorded after administration of 1 of 4 sedatives (acepromazine, butorphanol, xylazine, or detomidine). Serum drug concentrations were measured. Recordings were reviewed, states were identified, and representative EEG samples were analysed. These data were compared with data previously obtained during a study of natural sleep.

Results

Butorphanol was associated with brief episodes resembling slow wave sleep in 1 horse. Acepromazine led to SWS in 3 horses, including 1 that also exhibited rapid eye movement sleep. Periods of SWS were observed in all horses afer xylazine or detomidine administration. Normal sleep‐related EEG events and heart block, occurred in association with SWS regardless of which sedative was used. Spectral data varied primarily by state, but some differences were observed between sedative and natural data.

Conclusions and Clinical Importance

Qualitatively, EEG findings appeared identical whether sedation‐induced or naturally occurring. The startle response and heart block associated with some sedatives may be related to sleep. Alpha₂ agonists can be used to obtain high quality EEGs in horses, but acepromazine does not promote a relaxed state in all animals.     

Comparison of four drug combinations for total intravenous anesthesia of horses undergoing surgical removal of an abdominal testis

OBJECTIVE: To evaluate anesthetic effects of 4 drug combinations used for total intravenous anesthesia of horses undergoing surgical removal of an abdominal testis. DESIGN: Clinical trial. ANIMALS: 32 healthy cryptorchid horses. PROCEDURE: Horses were sedated with xylazine and butorphanol and were randomly assigned to 1 of 4 groups: induction of anesthesia with ketamine and diazepam and maintenance with bolus administration of ketamine and xylazine (KD/KX); induction and maintenance of anesthesia with bolus administration of tiletamine-zolazepam, ketamine, and detomidine (TKD); induction and maintenance of anesthesia with continuous infusion of xylazine, guaifenesin, and ketamine; and induction and maintenance of anesthesia with continuous infusion of guaifenesin and thiopental. Horses that moved 3 consecutive times in response to surgical stimulation or for which surgery time was > 60 minutes were administered an inhalant anesthetic, and data from these horses were excluded from analysis. RESULTS: Quality of induction was not significantly different among groups. Muscle relaxation and analgesia scores were lowest for horses given KD/KX, but significant differences among groups were not detected. Horses anesthetized with TKD had a significantly greater number of attempts to stand, compared with the other groups, and mean quality of recovery from anesthesia for horses in the TKD group was significantly worse than for the other groups. Anesthesia, surgery, and recovery times were not significantly different among groups. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that all 4 drug combinations can be used to induce short-term anesthesia for abdominal cryptorchidectomy in horses. However, horses receiving TKD had a poorer recovery from anesthesia, often requiring assistance to stand.     

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.     

Anesthetic, cardiorespiratory, and metabolic effects of four intravenous anesthetic regimens induced in horses immediately after maximal exercise

OBJECTIVE: To determine the anesthetic, cardiorespiratory, and metabolic effects of 4 IV anesthetic regimens 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. Each horse ran 4 simulated races, with a minimum of 14 days between races. Races were run at a treadmill speed that caused horses to exercise at 120% of their maximal oxygen consumption. Horses ran until fatigued or for a maximum of 2 minutes. Two minutes after exercise, horses received a combination of xylazine hydrochloride (2.2 mg/kg of body weight) and acepromazine maleate (0.04 mg/kg) IV. Five minutes after exercise, horses received 1 of the following 4 IV anesthetic regimens: ketamine hydrochloride (2.2 mg/kg); ketamine (2.2 mg/kg) and diazepam (0.1 mg/kg); tiletamine hydrochloride-zolazepam hydrochloride (1 mg/kg); and guaifenesin (50 mg/kg) and thiopental sodium (5 mg/kg). Treatments were randomized. Cardiopulmonary indices were measured, and samples of blood were collected before and at specific times for 90 minutes after each race. RESULTS: Each regimen induced lateral recumbency. The quality of induction and anesthesia after ketamine administration was significantly worse than after other regimens, and the duration of anesthesia was significantly shorter. Time to lateral recumbency was significantly longer after ketamine or guaifenesin-thiopental administration than after ketaminediazepam or tilet-amine-zolazepam administration. Arterial blood pressures after guaifenesin-thiopental administration were significantly lower than after the other regimens. CONCLUSIONS AND CLINICAL RELEVANCE: Anesthesia can be safely induced in sedated horses immediately after maximal exercise. Ketamine-diazepam and tilet-amine-zolazepam induced good quality anesthesia with acceptable perturbations in cardiopulmonary and metabolic indices. Ketamine alone and guaifenesin-thiopental regimens are not recommended.     

Xylazine-Ketamine and Detomidine-Tiletamine-Zolazepam Anesthesia in Horses

Eight horses were anesthetized three times, by intravenous administration of xylazine (1.1 mg/kg) and ketamine (2.2 mg/kg), detomidine (0.02 mg/kg) and tiletamine-zolazepam (1.1 mg/kg), or detomidine (0.04 mg/kg) and tiletamine-zolazepam (1.4 mg/kg). The sequences were randomized. The duration of analgesia and the times to sternal and standing positions were recorded. Heart rate, arterial pressure, pHa, PaCO2, and PaO2 were measured before and during anesthesia. The duration of analgesia with the two doses of detomidine-tiletamine-zolazepam, 26 +/- 4 minutes and 39 +/- 11 minutes, respectively, was significantly longer than the 13 +/- 6 minutes obtained with xylazine-ketamine. Bradycardia occurred after administration of detomidine, but heart rates returned to baseline values 5 minutes after administration of tiletamine and zolazepam. Arterial pressure was significantly higher and PaO2 significantly lower during anesthesia with detomidine-tiletamine-zolazepam than with xylazine-ketamine. Some respiratory acidosis developed with all anesthetic combinations. The authors conclude that detomidine-tiletamine-zolazepam can provide comparable anesthesia of a longer duration than xylazine and ketamine, but hypoxemia will develop in some horses.     

The effects of detomidine, romifidine or acepromazine on echocardiographic measurements and cardiac function in normal horses

OBJECTIVE: To evaluate by echo- and electrocardiography the cardiac effects of sedation with detomidine hydrochloride, romifidine hydrochloride or acepromazine maleate in horses. STUDY DESIGN: An experimental study using a cross-over design without randomization. ANIMALS: Eight clinically normal Standardbred trotters. MATERIALS AND METHODS: Echocardiographic examinations (two-dimensional, guided M-mode and colour Doppler) were recorded on five different days. Heart rate (HR) and standard limb lead electrocardiograms were also obtained. Subsequently, horses were sedated with detomidine (0.01 mg kg(-1)), romifidine (0.04 mg kg(-1)) or acepromazine (0.1 mg kg(-1)) administered intravenously and all examinations repeated. RESULTS: Heart rate before treatment with the three drugs did not differ significantly (p = 0.98). Both detomidine and romifidine induced a significant decrease (p < 0.001) in HR during the first 25 minutes after sedation; while acepromazine had a varying effect on HR. For detomidine, there was a significant increase in LVIDd (left ventricular internal diameter in diastole; p = 0.034) and LVIDs (left ventricular internal diameter in systole; p < 0.001). In addition, a significant decrease was found in IVSs (the interventricular septum in systole; p < 0.001), LVFWs (the left ventricular free wall in systole; p = 0.002) and FS% (fractional shortening; p < 0.001). The frequency of pulmonary regurgitation was increased significantly (p < 0.001). Romifidine induced a significant increase in LVIDs (p < 0.001) and a significant decrease in IVSs (p < 0.001) and FS% (p = 0.002). Acepromazine had no significant effect upon any of the measured values. CONCLUSIONS: and clinical relevance The results indicate that sedation of horses with detomidine and to a lesser extent romifidine at the doses given in this study has a significant effect on heart function, echocardiographic measurements of heart dimensions and the occurrence of valvular regurgitation. Although the clinical significance of these results may be minimal, the potential effects of sedative drugs should be taken into account when echocardiographic variables are interpreted in clinical cases.     

Prolongation of anesthesia with xylazine, ketamine, and guaifenesin in horses: 64 cases (1986-1989)

On 74 occasions, 54 horses and 6 foals were anesthetized with xylazine and ketamine or xylazine, guaifenesin, and ketamine, with or without butorphanol. On 64 occasions, anesthesia was prolonged for up to 70 minutes (34 +/- 15 min) by administration of 1 to 9 supplemental IV injections of xylazine and ketamine at approximately a third the initial dosage. All horses except 5 were positioned in lateral recumbency, and oxygen was insufflated. In adult horses, the time from induction of anesthesia to the first supplemental xylazine and ketamine injection was 13 +/- 4 minutes and the time between supplemental injections was 12.1 +/- 3.7 minutes. These results were consistent with predicted plasma ketamine concentration calculated from previously published pharmacokinetic data for ketamine in horses. Respiratory and heart rates and coccygeal artery pressure remained consistent for the duration of anesthesia. The average interval between the last injection of ketamine and assumption of sternal position was approximately 30 minutes, and was the same regardless of the number of supplemental injections. The time to standing was significantly longer (P less than 0.05) in horses given 2 supplemental injections, compared with those not given any or only given 1, but was not longer in horses given 3 supplemental injections. Recovery was considered unsatisfactory in 5 horses, but did not appear to be related to prolongation of anesthesia.     

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.     

Pharmacokinetics,pharmacodynamics, and metabolism of acepromazine following intravenous,oral, and sublingual administration to exercised Thoroughbred horses

Acepromazine is a tranquilizer used commonly in equine medicine. This study describes serum and urine concentrations and the pharmacokinetics and pharmacodynamics of acepromazine following intravenous, oral, and sublingual (SL) administration. Fifteen exercised adult Thoroughbred horses received a single intravenous, oral, and SL dose of 0.09 mg/kg of acepromazine. Blood and urine samples were collected at time 0 and at various times for up to 72 hr and analyzed for acepromazine and its two major metabolites (2‐(1‐hydroxyethyl) promazine and 2‐(1‐hydroxyethyl) promazine sulfoxide) using liquid chromatography–tandem mass spectrometry. Acepromazine was also incubated in vitro with whole equine blood and serum concentrations of the parent drug and metabolites determined. Acepromazine was quantitated for 24 hr following intravenous administration and 72 hr following oral and SL administration. Results of in vitro incubations with whole blood suggest additional metabolism by RBCs. The mean ± SEM elimination half‐life was 5.16 ± 0.450, 8.58 ± 2.23, and 6.70 ± 2.62 hr following intravenous, oral, and SL administration, respectively. No adverse effects were noted and horses appeared sedate as noted by a decrease in chin‐to‐ground distance within 5 (i.v.) or 15 (p.o. and SL) minutes postadministration. The duration of sedation lasted 2 hr. Changes in heart rate were minimal.     

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.     

Cardiopulmonary effects of xylazine and acepromazine in pregnant cows in late gestation

OBJECTIVE: To determine effects of sedation achieved by xylazine (XYL) or acepromazine (ACE) on cardiopulmonary function and uterine blood flow in cows in late gestation. ANIMALS: 8 cows between 219 and 241 days of gestation. PROCEDURE: Doses of ACE (0.02 mg/kg) or XYL (0.04 mg/kg) were administered IV. Measurements were obtained to determine cardiopulmonary effects and oxygen delivery to the uterus. RESULTS: Heart rate was not significantly affected by administration of ACE, but it decreased markedly after administration of XYL. Uterine artery flow was decreased at all times by XYL and was always less than for ACE. Xylazine increased uterine vascular resistance through 30 minutes and caused reduced PaO2 and increased PaCO2 at all time periods. Acepromazine caused a 5% decrease in PaO2 only at 5 minutes. Xylazine reduced oxygen delivery by 59% at 5 minutes and 32% at 45 minutes. In contrast, ACE caused a nonsignificant reduction of oxygen delivery by 16% at 15 minutes and a return to baseline values by 45 minutes CONCLUSIONS AND CLINICAL RELEVANCE: Xylazine markedly reduces flow and availability of oxygenated blood to the uterus, which may critically impair delivery of oxygen to the fetus at a stressful and important time of development or delivery. Acepromazine was associated with slight reductions of much shorter duration. When XYL is used to sedate pregnant cows, it could impose physiologic distress on the fetus and potentially increase fetal morbidity and mortality. When sedation of the dam is desirable, ACE could be an alternative to XYL.     

The use of atropine to control heart rate responses during detomidine sedation in horses

Detomidine is a sedative-analgesic which has a pharmacological profile similar to xylazine. There is evidence that the sedative effects are mediated through alpha-2 adrenoceptors.Cardiopulmonary responses were determined using detomidine as the principal agent and as a preanesthetic prior to the induction of general anesthesia. Compatibility with guaifenesin, sodium thia-mylal and halothane were determined.As in the case of xylazine, detomidine produces a slowing of heart rates. This was found to be either sinus bradycardia or heart block. There may be a corresponding increase in systolic blood pressures. The respiratory pattern is altered through the arterial blood gases and pH data supported evidence of adequate ventilation. The heart rate response to detomidine without anticholinergic treatment was transient and related to he duration of drug action.Atropine sulfate, 0.02 mg/kg i.v. was effective in preventing or treating bradycardia or heart block from detomidine. Heart rates also increased during the administration of guaifenesin and sodium thia-mylal when given 50 min poisit-detomidine.     

Tachypnea and Antipyresis in Febrile Horses after Sedation with α2‐Agonists

Background: Signs of tachypnea after sedation of febrile horses with α₂‐agonists have been noted previously but have not been further investigated. Objectives: To examine the effects of xylazine and detomidine on respiratory rate and rectal temperature in febrile horses and to investigate if either drug would be less likely than the other to cause changes in these variables. Animals: Nine febrile horses and 9 healthy horses were included in the study. Methods: Horses were randomly assigned to sedation with xylazine 0.5 mg/kg or detomidine 0.01 mg/kg. Heart rate and respiratory rate were recorded before sedation and at 1, 3, and 5 minutes after injection. Hourly measurements of rectal temperature were performed starting before sedation. Results: All febrile horses experienced an episode of tachypnea and antipyresis after sedation. Rectal temperature in the febrile group was significantly lower at 1, 2, and 3 hours after sedation. In several measurements, the decrease was >1°C. Respiratory rate in the febrile group was significantly increased after sedation. All febrile horses were breathing >40 breaths/min and 3 horses >100 breaths/min 5 minutes after sedation. No differences were noted between the 2 treatments. No significant changes in respiratory rate or temperature were noted in the reference group. Conclusions and Clinical Importance: Febrile horses can become tachypneic after sedation with detomidine or xylazine. The antipyretic properties of α₂‐agonists need consideration when evaluating patients that have been sedated several hours before examination.     

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.     

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.     

Does the induction agent affect the course of halothane anaesthesia in horses?

Four hundred and ninety horses were anaesthetised with halothane for clinical surgical or diagnostic procedures following induction with either detomidine/keta-mine, detomidine/thiopentone, xylazine/ketamine or guaiphenesin/thiopentone. Routine clinical monitoring was performed during anaesthesia. All horses developed hypotension (mean arterial pressures below 80 mm Hg) and respiratory depression (significant fall in respiratory rate and arterial carbon dioxide tension above 7 kPa (53 mm Hg)) consistent with the recognised effects of halothane. All anaesthetic procedures incorporating xylazine or detomidine resulted in lower pulse rates (28–35 per min) than after guaiphenesin/thiopentone (36–44 per min) and there was greater respiratory depression after techniques employing thiopentone rather than keta-mine. Development of hypotension was delayed after techniques using the α₂ adrenoceptor agonist agents (xylazine and detomidine), particularly detomidine. Prernedication with acepromazine did not affect any of the physiological variables measured after techniques employing detomidine. Recovery to standing was fastest after xylazine/ketamine (31±1 min) and slowest after detomidine/thiopentone (53±2 min). Recovery quality was best after detomidine/thiopentone and all techniques employing an α₂ adrenoceptor agonist agent resulted in smoother recovery than after guaiphenesin/thiopentone. This study demonstrates that most of the physiological effects of individual induction agents are overridden by the cardiovascular and respiratory depressant effects of halothane. The study also shows that detomidine is an acceptable sedative for use before general anaesthesia with halothane in horses.