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.     

A comparison of the sedative effects of three α2-adrenoceptor agonists (romifidine, detomidine and xylazine) in the horse

The sedative effects of a new alpha 2-adrenoceptor agonist, romifidine, were compared with those of xylazine and detomidine. Five horses were treated with two doses of romifidine (40 micrograms/kg body weight and 80 micrograms/kg body weight), two doses of detomidine (10 micrograms/kg body weight and 20 micrograms/kg body weight) and one dose of xylazine (1 mg/kg body weight) given by intravenous injection using a Latin-square design. The dose of 80 micrograms/kg romifidine appeared equipotent to 1 mg/kg xylazine and 20 micrograms/kg detomidine, although at these doses both xylazine and detomidine had a shorter action. Detomidine 20 micrograms/kg and xylazine both produced greater lowering of the head and a greater degree of ataxia than romifidine at either dose. Romifidine produced sedation similar to that of the other drug regimes. The effect upon imposed stimuli was similar.     

Hemodynamic effects of xylazine in the calf

The hemodynamic effects of sedative level doses of xylazine in five chronically instrumented calves were studied. These effects included immediate and prolonged reductions in heart rate, cardiac output, arterial blood pressure, and left ventricular dp/dt max. Stroke volume showed an initial decrease in value with a return in 15 minutes to base-line values. Total peripheral resistance, end-diastolic left ventricular pressure, end-diastolic left ventricular volume, and left ventricular residual fraction were increased after drug administration. The results indicate that a depressed myocardium results from xylazine administration. With one exception (the absence of a hypertensive response), these effects largely parallel, both quantitatively and qualitatively, those seen with this drug in other species. Sedation by xylazine is produced in cattle at doses which are small compared to those which is required for sedation in other species. These same small doses in cattle also cause hemodynamic changes.     

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.     

Effects of xylazine, medetomidine, detomidine, and diazepam on sedation, heart and respiratory rates, and cloacal temperature in rock partridges (Alectoris graeca).

In this study, heart and respiratory rates, cloacal temperature, and quality of sedation were evaluated before (0 min) and after (10, 20, and 30 min) i.m. administration of xylazine (10 mg/kg; n = 7), medetomidine (75 li; n = 6), detcmidine (0.3 mg/kg; n = 6), or diazepam (6 mg/kg; n = 7) in rock partridges (Alectoris graeca). All partridges recovered from sedation without any disturbance. Xylazine and diazepam administration did not induce significant changes in heart rate, which did decrease significantly after medetomidine and detomidine administration (P < 0.001). Mean respiratory rate was decreased dramatically at 20 and 30 min after xylazine (P < 0.001) and medetomidine (P < 0.005) administration, and at all stages of sedation after detomidine injection (P < 0.001), whereas there was not any significant change after diazepam injection. In all groups, cloacal temperature measured at 10, 20, and 30 min tended to decrease compared with baseline values. Sedative effects of the drugs started within 2.1+/-0.2 min for detomidine, 2.6 +/- 0.4 min for diazepam, 3.1 -+/-.4 min for xylazine, and 4.8+/-0.8 min for medetomidine application. There was an extreme variability in time to recovery for each drug: 205 +/-22.2 min for xylazine, 95 -12.2 min for medetomidine, 260+/-17.6 min for detomidine, and 149 + 8.3 min for diazepam. In conclusion, xylazine, medetomidine, detomidine, and diazepam produced sedation, which could permit some clinical procedures such as handling and radiographic examination of partridges to occur. Of the four drugs, xylazine produced stronger and more efficient sedation compared to the others, which could permit only minor procedures to be performed. However, depending on the drug used, monitoring of heart and respiratory rates and cloacal temperature might be required.     

Evaluation of the sedative and clinical effects of xylazine,detomidine, medetomidine and dexmedetomidine in miniature donkeys

ABSTRACT

Aim: To evaluate the sedative and clinical effects of I/V xylazine, detomidine, medetomidine and dexmedetomidine in miniature donkeys.

Methods: Seven clinically healthy, male adult miniature donkeys with a mean age of 6 years and weight of 105?kg, were assigned to five I/V treatments in a randomised, cross-over design. They received either 1.1?mg/kg xylazine, 20?μg/kg detomidine, 10?μg/kg medetomidine, 5?μg/kg dexmedetomidine or saline, with a washout period of ≥7 days. The degree of sedation was scored using a 4-point scale by three observers, and heart rate (HR), respiration rate (RR), rectal temperature and capillary refill time (CRT) were recorded immediately before and 5, 10, 15, 30, 60, 90 and 120 minutes after drug administration.

Results: All saline-treated donkeys showed no sedation at any time, whereas the donkeys treated with xylazine, detomidine, medetomidine and dexmedetomidine had mild or moderate sedation between 5 and 60 minutes after treatment, and no sedation after 90 minutes. All animals recovered from sedation without complication within 2 hours. The mean HR and RR of saline-treated donkeys did not change between 0 and 120 minutes after administration, but the mean HR and RR of donkeys treated with xylazine, detomidine, medetomidine and dexmedetomidine declined between 5 and 60 minutes after drug administration. The mean rectal temperature of all treated donkeys did not change between 0 and 120 minutes after administration. The CRT for all donkeys was ≤2 seconds at all times following each treatment.

Conclusions and clinical relevance: Administration of xylazine at 1.1?mg/kg, detomidine at 20?μg/kg, medetomidine at 10?μg/kg and dexmedetomidine at 5?μg/kg resulted in similar sedation in miniature donkeys. Therefore any of the studied drugs could be used for sedation in healthy miniature donkeys.     

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.     

Ketamine, Telazol, xylazine and detomidine. A comparative anesthetic drug combinations study in ponies.

This study was designed to assess the effects of 5 anesthetic drug combinations in ponies: (1) ketamine 2.75 mg/kg, xylazine 1.0 mg/kg (KX), (2) Telazol 1.65 mg/kg, xylazine 1.0 mg/kg (TX), (3) Telazol 2 mg/kg, detomidine 20 micrograms/kg (TD-20), (4) Telazol 2 mg/kg, detomidine 40 micrograms/kg (TD-40), (5) Telazol 3 mg/kg, detomidine 60 micrograms/kg (TD-60). All drugs were given iv with xylazine or detomidine preceding ketamine or Telazol by 5 min. Heart rate was decreased significantly from 5 min to arousal after TD-20 but only at 60 and 90 min after TD-40 and TD-60 respectively. Respiratory rate was decreased significantly for all ponies. Induction time did not differ between treatments. Duration of analgesia was 10 min for KX, 22.2 min for TX, 27.5 min for TD-20, 32.5 min for TD-40, and 70 min for TD-60. Arousal time was significantly longer with detomidine and Telazol. Smoothness of recovery was judged best in ponies receiving KX and TD-40. All ponies stood unassisted 30 min after signs of arousal.     

Influence of yohimbine and tolazoline on the cardiovascular, respiratory, and sedative effects of xylazine in the horse

To determine the effects of yohimbine and tolazoline on the cardiovascular, respiratory and sedative effects of xylazine, four horses were sedated with xylazine and treated with either yohimbine, tolazoline or saline. Xylazine was administered as an intravenous (i.v.) bolus (1.0 nig/kg) followed by a continuous infusion at the rate of 12 μg/kg/min. Heart rate, respiratory rate, mean arterial pressure, arterial blood gases, and the chin-to-floor distance were recorded throughout the experiment. After 60 min, either yohimbine or tolazoline was administered i.v. in incremental doses until reversal of sedation (defined as the return of the chin-to-floor distance to baseline values) was achieved. A control group in which a saline bolus was administered instead of an antagonist drug was included for comparison.
The average dose of yohimbine administered was 0.12 ± 0.02 (SEM) mg/kg. While the average dose of tolazoline was 7.5 ± 1.1 mg/kg. Both tolazoline and yohimbine antagonized the ventricular bradycardia and A-V conduction disturbances observed with xylazine administration. No change in mean arterial pressure was observed with xylazine or yohimbine administration, but tolazoline caused persistent mild systemic hypertension. There were no clinically significant changes in respiratory rate or arterial blood gas values with administration of either xylazine, yohimbine or tolazoline. The chin-to-floor distance decreased significantly with xylazine administration and increased significantly with administration of either yohimbine or tolazoline. In conclusion, both yohimbine and tolazoline successfully antagonized the cardiovascular and CNS depression associated with xylazine administration.     

Haemodynamic changes during sedation in ponies

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (greater than 90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal. alpha 2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 micrograms/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation. Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the alpha 2-agonistic sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance. The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.     

Cardiopulmonary effects of romifidine/ketamine or xylazine/ketamine when used for short duration anesthesia in the horse

The cardiovascular changes associated with anesthesia induced and maintained with romifidine/ketamine versus xylazine/ ketamine were compared using 6 horses in a cross over design. Anesthesia was induced and maintained with romifidine (100 microg/kg, IV)/ketamine (2.0 mg/kg, IV) and ketamine (0.1 mg/kg/min, IV), respectively, in horses assigned to the romifidine/ ketamine group. Horses assigned to the xylazine/ketamine group had anesthesia induced and maintained with xylazine (1.0 mg/kg, IV)/ketamine (2.0 mg/kg, IV) and a combination of xylazine (0.05 mg/kg/min, IV) and ketamine (0.1 mg/kg/min, IV), respectively. Cardiopulmonary variables were measured at intervals up to 40 min after induction. All horses showed effective sedation following intravenous romifidine or xylazine and achieved recumbency after ketamine administration. There were no significant differences between groups in heart rate, arterial oxygen partial pressures, arterial carbon dioxide partial pressures, cardiac index, stroke index, oxygen delivery, oxygen utilization, systemic vascular resistance, left ventricular work, or any of the measured systemic arterial blood pressures. Cardiac index and left ventricular work fell significantly from baseline while systemic vascular resistance increased from baseline in both groups. The oxygen utilization ratio was higher in the xylazine group at 5 and 15 min after induction. In conclusion, the combination of romifidine/ketamine results in similar cardiopulmonary alterations as a xylazine/ketamine regime, and is a suitable alternative for clinical anesthesia of the horse from a cardiopulmonary viewpoint.     

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.     

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.     

The parasympatholytic effects of atropine sulfate and glycopyrrolate in rats and rabbits.

Nine groups of rats (n = 5 per group) received an intramuscular (IM) injection of one of the following drugs or drug combinations: saline, atropine (0.05 mg/kg), glycopyrrolate (0.5 mg/kg), ketamine:xylazine (85:15 mg/kg), ketamine:detomidine (60:10 mg/kg), atropine:ketamine:xylazine (0.05: 85:15 mg/kg), glycopyrrolate: ketamine:xylazine (0.5:85:15 mg/kg), atropine:ketamine:detomidine (0.05: 60:10 mg/kg) or glycopyrrolate: ketamine:detomidine (0.5:60:10). Similarly six groups of rabbits (n = 5) received an IM injection of either saline, atropine (0.2 mg/kg), atropine (2 mg/kg), glycopyrrolate (0.1 mg/kg), ketamine:xylazine (35:10 mg/kg) or glycopyrrolate:ketamine:xylazine (0.1:35:10 mg/kg). In rats, atropine sulfate (0.05 mg/kg) and glycopyrrolate (0.5 mg/kg) produced an increase in heart rate for 30 and 240 min, respectively. In rabbits atropine sulfate at either 0.2 or 2.0 mg/kg did not induce a significant increase in heart rate, but glycopyrrolate (0.1 mg/kg) elevated the heart rate above saline treated animals for over 50 min. Both atropine and glycopyrrolate provided protection against a decrease in heart rate in rats anesthetized with ketamine: xylazine (85:15 mg/kg) or ketamine: detomidine (60:10 mg/kg); however, glycopyrrolate was significantly more effective in maintaining the heart rate within the normal range. Glycopprrolate also prevented a decrease in heart rate in rabbits anesthetized with ketamine:xylazine (35:5 mg/kg). Neither glycopyrrolate nor atropine influenced respiration rate, core body temperature or systolic blood pressure when used alone or when combined with the injectable anesthetic. Glycopyrrolate is an effective anticholinergic agent in rabbits and rodents and more useful as a preanesthetic agent than atropine sulfate in these animals.     

The Reliability of Two Different Protocols for Pharmacologically Induced Ejaculation in Donkeys (Equus asinus)

The aim of this study was to pharmacologically induce ejaculation in male donkeys. Two methods for pharmacological ejaculation were used. The first method was the administration of xylazine (0.66 mg/kg, intravenous); the second method was the administration of detomidine chloride (0.02 mg/kg, intramuscular), and when ejaculation was not achieved in 15 minutes, the administration of a half dose of detomidine chloride (0.01 mg/kg, intramuscular) was repeated. Both of these methods were used in all animals. In the study, 10 male donkeys were used. After the administration of xylazine, no ejaculation was observed. After the administration of detomidine, ejaculation was achieved in 20% of the cases (2 of 10). We assume that these methods are not satisfactory for ex-copula induction of ejaculation in male donkeys.     

Xylazine and a xylazine/fentanyl citrate/azaperone combination in farmed deer. I: dose rate comparison

Six 1-year-old farmed red deer were used to compare physiological and behavioural responses to a range of doses of 5% xylazine with or without the addition of 0.4 mg of fentanyl citrate and 3.2 mg of azaperone per ml. Each deer was randomly assigned to one of six treatments: xylazine alone at 0.4 and 0.6 mg/kg, the xylazinelfentanyl citrate/azaperone combination containing 0.2, 0.4 and 0.6 mg/kg of xylazine, or a sterile water control. Injections were given intramuscularly in the anterior neck, operator blind, on each of 6 sampling days between October and January, such that each deer received all treatments with 9-28 days between each treatment. Measurements included heart rate and respiration rate. A 0-3 scoring system (normal to nil response, respectively) was devised to record sedative responses (body stance, head position, degree of eye closure, palpebral reflex, resistance to movement of the head, response to noise) and analgesic responses to touch and pinching of the ear, and response to a needle prick in the gluteal region. Scores were added to produce a sedation score and analgesia score, respectively, for each treatment. Records were taken immediately prior to injection and thereafter at 5, 14, 25, 35, 60, 90, 120, 150, 180, 210, 240 and 300 minutes. All deer given each dose rate of the xylazine and the xylazine/fentanyl citrate/azaperone combination became recumbent. There was a tendency for the time to recumbency and variation of time to recumbency to be shorter at higher dose rates and with the addition of fentanyl citrate and azaperone to xylazine, particularly with xylazine at 0.4 mg/kg. These trends were not statistically significant (p>0.05). The duration of recumbency was shorter with the low dose of the xylazine/fentanyl trateiazaperone combination (0.2 mg/kg of xylazine) than for the higher doses of xylazine alone or the combination of drugs (p<0.05). There were no significant differences in heart rates or respiration rates between treatments, although all treatments significantly reduced both heart and respiration rates (p<0.01). The sedation scores showed similar peak responses and timing to peak responses (14-25 min) to both drug treatments and all dose rates, but the responses were less persistent for lower doses. The analgesia scores showed a similar pattern, with peak responses 14-35 minutes after administration and more persistence at higher dose rates of both xylazine alone and the xylazine/fentanyl citrate/azaperone combination. This study has shown that most physiological and behavioural responses to a range of doses of xylazine or the xylazine/fentanyl citrate/azaperone combination were statistically similar. However, there was a tendency for recumbency to occur more rapidly and with less variation in timing when the mid-range dose of the drug combination was used, supporting the observation by practitioners that the drug combination results in a more rapid and reliable state of recumbency at a lower dose rate of xylazine.     

Influence of idazoxan on the respiratory blood gas changes induced by alpha 2-adrenoceptor agonist drugs in conscious sheep

Administration of either xylazine (50 micrograms/kg) or detomidine (10 micrograms/kg) caused a significant degree of arterial hypoxaemia in six conscious sheep. This effect was independent of any changes produced by changes in posture as all the sheep remained standing. Administration of the specific alpha 2-antagonist drug idazoxan (0.1 mg/kg bodyweight) five minutes before injection of either of the drugs completely abolished the hypoxaemia. These results lend support to the view that the respiratory effect of these drugs is mediated via alpha 2-adrenoceptor activity.     

Influence of detomidine on echocardiographic function parameters and cardiac hemodynamics in horses with and without heart murmur

30 warmblood horses were examined before and after sedation with 20 micrograms/kg BW detomidine, to determine changes of cardiac function parameters, using B-mode, M-mode and Doppler echocardiography. 15 horses showed a heart murmur, but no clinical signs of cardiac heart failure, 15 horses had neither a heart murmur nor other signs of cardiac disease. After sedation with detomidine we could recognise a significant increase of end-diastolic left atrium diameter, an increase of end-systolic left ventricular diameter and aortic root diameter. The end-systolic thickness of papillary muscle and interventricular septum showed a decrease. Fractional shortening and amplitude of left ventricular wall motion was decreased after sedation. The mitral valve echogram revealed a presystolic valve closure and an inflection in the Ac slope (B-notch) in xy horses before sedation. Both increased after sedation with detomidine. Doppler echocardiography showed a decrease of blood flow velocity and velocity time integral (VTI) in the left and right ventricular outflow tract after sedation. Regurgitant flow signals were intensified following sedation in xy horses, especially at the mitral valve.     

Cardiovascular and respiratory effects of acetylpromazine and xylazine on halothaneanesthetized horses

Circulatory and respiratory effects of intravenously administered acetylpromazine (0.033 and 0.067 mg/kg) and xylazine (0.5 and 1.0 mg/kg) were studied in drug cross-over fashion in eight laterally recumbent horses anesthetized only with halothane (1.06%, end-tidal) in O2. Both doses of acetylpromazine caused a significant and sustained elevation in cardiac output via a rise in stroke volume. Xylazine produced an initial significant fall in cardiac output followed by a return to control levels. Halothane anesthesia did not prevent xylazine-related atrioventricular conduction block. All treatments caused a similar significant fall in arterial blood pressure (acetylpromazine, total peripheral resistance-related; xylazine, cardiac output-related). PaCO2 significantly increased after all treatments. PaCO2 decreased significantly only following xylazine treatment. One horse (not included in the tabulation) developed ventricular fibrillation and died 15 min after receiving its first injection (0.5 mg/kg) of xylazine.     

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.