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.     

Effects of idazoxan, tolazoline, and yohimbine on xylazine-induced respiratory changes and central nervous system depression in ewes

We compared the ability of 3 alpha 2-adrenoreceptor antagonists, idazoxan (0.05 mg/kg), tolazoline (2 mg/kg), and yohimbine (0.2 mg/kg) to reverse xylazine (0.3 mg/kg)-induced respiratory changes and CNS depression in 6 ewes. Once weekly, each ewe was given a random IV treatment of xylazine, followed in 5 minutes by either an antagonist or 0.9% NaCl solution. Xylazine alone caused recumbency for 54.2 +/- 5.3 minutes (mean +/- SEM). Xylazine also increased respiratory rate and decreased PaCO2 for at least 45 minutes, but did not significantly change arterial pH or PaCO2. Idazoxan and tolazoline were equally effective in reversing the respiratory actions of xylazine; however, yohimbine was less effective in reducing the respiratory rate and was ineffective in antagonizing the decreased PaO2. Idazoxan and tolazoline decreased the duration of xylazine-induced recumbency to 6.3 +/- 0.6 and 9.5 +/- 2.3 minutes, respectively, whereas yohimbine did not significantly change this effect of xylazine. Thus, at the dosages studied, idazoxan and tolazoline appeared to be more effective than yohimbine in reversing the respiratory and CNS depressant actions of xylazine in sheep.     

Effects of xylazine on cecal mechanical activity and cecal blood flow in healthy horses

Mechanical activity of the cecal body, lateral cecal arterial blood flow, carotid arterial pressure, and heart rate were measured in 6 conscious healthy horses 30 minutes before and for 120 minutes after IV administration of xylazine at dosages of 1.1 mg/kg of body weight, 0.55 mg/kg, and 0.275 mg/kg. Xylazine at a dosage of 1.1 mg/kg reduced the mean motility index (the product of the mean amplitude of contractions and the total duration of contractile activity divided by the recording time) of the circular and longitudinal muscle layers for the first, second, third, and fourth 30-minute periods after administration of xylazine. Xylazine at a dosage of 0.55 mg/kg reduced the motility index of the circular and longitudinal muscle layers for the first and second 30-minute periods after administration of xylazine. Xylazine at a dosage of 0.275 mg/kg reduced the motility index of the circular and longitudinal muscle layers for the first 30-minute period after administration of xylazine. Mean lateral cecal arterial blood flow was significantly (P less than 0.05) lower than the base-line value at 2 and 4 minutes after administration of all 3 xylazine dosages and at 8 minutes after administration of xylazine dosages of 1.1 mg/kg and 0.55 mg/kg. All dosages of xylazine caused transient hypertension and bradycardia, followed by hypotension.     

Anesthesia of wood bison with medetomidine-zolazepam/tiletamine and xylazine-zolazepam/tiletamine combinations

This study was designed to evaluate 2 combinations for immobilization of bison. Seven wood bison received 1.5 mg/kg body weight (BW) of xylazine HCl + 1.5 mg/kg BW of zolazepam HCl and 1.5 mg/kg BW of tiletamine HCl on one occasion. The bison received 60 micrograms/kg BW of medetomidine HCl + 0.6 mg/kg BW of zolazepam HCl and 0.6 mg/kg BW of tiletamine HCL on another occasion. Xylazine was antagonized with 3 mg/kg BW of tolazoline HCl and medetomidine HCl was antagonized with 180 micrograms/kg (BW) of atipamezole HCl. Temporal characteristics of immobilization and physiological effects (acid-base status, thermoregulatory, cardiovascular, and respiratory effects) of the drug combinations were compared. Induction was significantly faster with xylazine HCl-zolazepam HCl/tiletamine HCl. Recovery following antagonist administration was significantly faster with medetomidine HCl-zolazepam HCl/tiletamine HCl. The average drug volumes required were 7.00 mL of xylazine HCl-zolazepam HCl/tiletamine HCL and 2.78 mL of medetomidine HCl-zolazepam HCl/tiletamine HCl. Hypoxemia, hypercarbia, and rumenal tympany were the major adverse effects with both drug combinations.     

Antagonistic effect of atipamezole on xylazine-induced sedation, bradycardia, and ruminal atony in calves.

Three doses of an alpha 2-adrenoreceptor antagonist, atipamezole, were administered to reverse xylazine-induced sedation, bradycardia, and ruminal atony in calves. Once a week for 4 weeks, each of 6 calves was administered IV 1 treatment of: 0.3 mg of xylazine/kg of body weight, followed in 10 minutes by 1 ml of 0.9% NaCl; 0.3 mg of xylazine/kg, followed in 10 minutes by 3 micrograms of atipamezole/kg; 0.3 mg of xylazine/kg, followed in 10 minutes by 10 micrograms of atipamezole/kg; or 0.3 mg of xylazine/kg, followed in 10 minutes by 30 micrograms of atipamezole/kg. The order of the 4 treatments in each calf was selected at random. Xylazine alone caused lateral recumbency for 33.6 +/- 7.1 minutes (mean +/- SEM). Atipamezole administered at dosages of 3, 10, and 30 micrograms/kg shortened xylazine-induced lateral recumbency to 20.5 +/- 3.0, 10.2 +/- 0.2, and 9.3 +/- 0.5 minutes, respectively. Calves given xylazine alone stood at greater than 60 minutes after the onset of recumbency. Atipamezole given at 3, 10, and 30 micrograms/kg shortened the time from onset of lateral recumbency to standing to 40.2 +/- 6.9, 12.8 +/- 1.1, and 10.0 +/- 0.7 minutes, respectively. Drowsiness was found in calves given the lowest dosage of atipamezole (3 micrograms/kg) after the calves stood. Atipamezole given at dosages of 10 and 30 micrograms/kg reversed xylazine-induced ruminal atony in a dose-dependent manner. In addition, 30 micrograms of atipamezole/kg reversed xylazine-induced bradycardia, but the lower dosages of this antagonist did not. Results indicated that 30 micrograms of atipamezole/kg should be a useful antidote for xylazine overdose in cattle.     

Cardiorespiratory Effects of the Intravenous Administration of Tiletamine-Zolazepam to Dogs

The anesthetic, hemodynamic, and respiratory effects of an intravenously administered 1:1 combination of tiletamine and zolazepam were evaluated in dogs. Each dog received tiletamine-zolazepam (6.6, 13.2, 19.8 mg/kg) on two occasions, once when awake and a second time with residual isoflurane anesthesia while instrumented for the recording of hemodynamic data. Tiletamine-zolazepam administered to conscious dogs resulted in good, rapid induction of anesthesia. Time to sternal recumbency (recovery) was dose-dependent. Character of recovery tended to be better with the lower dose. Tiletamine-zolazepam caused significant increases in heart rate after all doses and significant increases in cardiac output after the two larger doses. All doses caused significant decreases in arterial blood pressure at 1 minute. Arterial blood pressures returned to baseline and then increased significantly above baseline values. The rate of development of left ventricular pressure was significantly decreased 1 minute after the two higher doses, returned to normal, and then was significantly increased above baseline for all doses. Peripheral vascular resistance increased transiently 1 minute after the 6.6 mg/kg dose. Peripheral vascular resistance decreased significantly after the 13.2 and 19.8 mg/kg doses. Minute ventilation was significantly decreased only after the 19.8 mg/kg dose.     

Evaluation of Three Midazolam-Xylazine Mixtures Preliminary Trials in Dogs

The depressant effects of midazolam and xylazine on the central nervous system (CNS) were evaluated in 12 dogs. Xylazine was administered to six dogs (1.1 mg/kg intravenously [IV]) followed in 5 minutes by midazolam (1.0 mg/kg intramuscularly [IM]). In a second group of six dogs, xylazine (2.2 mg/kg IM) was followed in 5 minutes by midazolam (1.0 mg/kg IV). Both drug regimens induced rapid and profound sedation or anesthesia. Duration of action varied with the doses and routes of administration. Dogs given the high dose of xylazine IM had an arousal time of 95.4 +/- 8.9 minutes and a walking time of 155.4 +/- 8.8 minutes. These values exceeded the IV xylazine values threefold. Partial reversal of CNS depression was accomplished with either a benzodiazepine antagonist (flumazenil) or an alpha-2 antagonist (yohimbine). In a separate trial, a mixture of xylazine (0.55 mg/kg), midazolam (1.0 mg/kg), and butorphanol (0.1 mg/kg) with and without glycopyrrolate was evaluated in eight dogs. As with the xylazine-midazolam combinations, the CNS depressant effect of this mixture was clinically indistinguishable from anesthesia achieved with other rapid-acting injectable agents. Clinical signs of CNS depression were readily and completely antagonized by the simultaneous injection of flumazenil and yohimbine.     

Antagonism of xylazine sedation in steers by doxapram and 4-aminopyridine

Five groups of 6 fasted crossbred steers were injected IM with standard dosages of xylazine hydrochloride (0.3 to 0.5 mg/kg). At maximal sedation, the steers were injected IV with the antagonists' doxapram (1.0 mg/kg), doxapram + yohimbine (0.125 mg of yohimbine/kg), doxapram + 4-aminopyridine (4-AP; 0.3 mg of 4-AP/kg), or 4-AP + yohimbine. One group was given 1.0 ml of saline solution IV instead of antagonists. Doxapram, doxapram + yohimbine, doxapram + 4-AP, and 4-AP + yohimbine decreased mean standing time (time from antagonist injection until animal could stand unaided) to 17.0, 4.3, 3.3, and 4.5 minutes, respectively--significantly (P less than 0.05) down from a control value of 49.8 minutes. Mean total recovery time (time from xylazine injection until animal resumed eating) was decreased to 78 minutes by doxapram and 81.6 minutes by doxapram + 4-AP--significantly (P less than 0.05) down from the control value of 142.9 minutes. Respiratory character was improved (depth of respiration was increased) only by doxapram + 4-AP. Relapses to recumbency and marked sedation were not seen in steers given doxapram + 4-AP or the saline solution. One steer given doxapram, 2 given doxapram + yohimbine, and 1 given 4-AP + yohimbine relapsed to recumbency and sedation. Recovery was relatively smooth in steers given doxapram + 4-AP or 4-AP + yohimbine. Animals given doxapram or doxapram + yohimbine had difficult recoveries.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antagonistic effect of idazoxan on xylazine-induced central nervous system depression and bradycardia in calves

Two doses of an alpha 2-adrenoreceptor antagonist, idazoxan, were administered to reverse the CNS depressant and bradycardia effects of xylazine in calves. Once a week for 3 weeks, each of 6 calves were administered IV one treatment of: (1) 0.2 mg of xylazine/kg of body weight followed in 10 minutes by 1 ml of 0.9% NaCl, (2) 0.2 mg of xylazine/kg followed in 10 minutes by 10 micrograms of idazoxan/kg, or (3) 0.2 mg of xylazine/kg followed in 10 minutes by 30 micrograms of idazoxan/kg. The order of the 3 treatments in each calf was selected at random. Xylazine alone caused lateral recumbency for 27.2 +/- 3.0 minutes (mean +/- SEM). Idazoxan administered at dosages of 10 and 30 micrograms/kg shortened xylazine-induced lateral recumbency to 11.5 +/- 0.8 and 10.3 +/- 0.2 minutes, respectively. Calves given xylazine alone stood at greater than 60 minutes after the onset of recumbency. Idazoxan given at dosages of 10 and 30 micrograms/kg shortened the time to standing to 16.8 +/- 1.7 and 11.3 +/- 0.2 minutes, respectively. Idazoxan given at a dosage of 30 micrograms/kg also reversed xylazine-induced bradycardia. Results indicated that idazoxan should be a useful antidote for xylazine overdose in cattle.     

Antagonistic effect of atipamezole, flumazenil and naloxone following anaesthesia with xylazine, tramadol and tiletamine/zolazepam combinations in pigs

ObjectiveTo evaluate the antagonistic effects of atipamezole (ATI), flumazenil (FLU) and naloxone (NAL) alone and in various combinations following administration of tiletamine–zolazepam–xylazine–tramadol.Study designProspective, experimental, randomized cross-over study.AnimalsEight Chinese miniature pigs (three females and five males) mean age 8 (range 7–10) months and bodyweight 57.5 (52.4–62.1) kg.MethodsAll animals were anaesthetized with tiletamine/zolazepam (3.0 mg kg^?1), xylazine (1.2 mg kg^?1) and tramadol (1.6 mg kg^?1) given intramuscularly (IM). Thirty minutes later, one of eight treatments was administered IM: saline control, ATI (0.12 mg kg^?1), FLU (0.1 mg kg^?1), NAL (0.03 mg kg^?1), ATI–FLU, FLU–NAL, ATI–NAL or ATI–FLU–NAL. After injection of antagonists the following times were recorded: to recovery of the palpebral, pedal and tail clamp reflexes, to head movement, sternal recumbency, standing and walking. Posture, sedation, analgesia, jaw relaxation and auditory response were scored at set times until 120 minutes after injection of antagonists. Heart rates, respiratory rates and rectal temperature were measured at those times. Data were analyzed by anova for repeated measures, followed by the Tukey’s test to compare differences between means, or by Kruskal–Wallis test as appropriate.ResultsFLU, NAL alone, or FLU–NAL did not effectively antagonize anaesthesia induced by tiletamine/zolazepam–xylazine–tramadol. ATI, ATI–FLU, ATI–NAL and ATI–FLU–NAL produced an immediate and effective recovery from anaesthesia. The combination of ATI–FLU–NAL was the most effective combination in antagonizing the anaesthetic effect. Adverse effects such as tachycardia, tachypnoea, excitement and muscle tremors were not observed during this study.Conclusion and clinical relevanceATI–FLU–NAL is the most effective combination for antagonizing tiletamine/zolazepam–xylazine–tramadol anaesthesia in pigs. However, ATI alone or in various combinations also provides effective antagonism.     

Effects of tolazoline and yohimbine on xylazine-induced central nervous system depression, bradycardia, and tachypnea in sheep

We compared the ability of tolazoline and yohimbine to antagonize xylazine-induced central nervous system depression, bradycardia, and tachypnea in 9 ewes and 5 rams. Once a week for 3 weeks, each sheep received one IV treatment of 0.4 mg xylazine/kg, 0.4 mg xylazine/kg followed in 10 minutes by 2 mg tolazoline/kg, or 0.4 mg xylazine/kg followed in 10 minutes by 0.2 mg yohimbine/kg. The order of the 3 treatments in each sheep was randomized. Xylazine alone caused recumbency for 41.0 +/- 3.7 minutes (mean +/- SEM). Tolazoline and yohimbine shortened the xylazine-induced recumbency to 12.1 +/- 0.9 minutes and 18.1 +/- 1.5 minutes, respectively. Sheep given xylazine alone had head droop for 34.0 +/- 5.4 minutes after rising. Head drooping of sheep given tolazoline or yohimbine was reduced to 10.1 +/- 1.7 minutes and 14.2 +/- 1.7 minutes, respectively. Both tolazoline and yohimbine reversed the bradycardia and tachypnea that followed xylazine administration. No statistical differences in the rate and magnitude of the reversal were observed between the 2 drugs.     

Antagonism of xylazine sedation with yohimbine, 4-aminopyridine, and doxapram in dogs

Groups of atropinized dogs (6 dogs/group) were sedated with xylazine (2.2 mg/kg of body weight, IM). At recumbency, the dogs were given IV saline solution (control groups), yohimbine (0.05, 0.1, and 0.2 mg/kg), 4-aminopyridine (4-AP; 0.3, 0.6, and 0.9 mg/kg), doxapram (0.5, 1.0, 2.0, and 4.0 mg/kg), or the smallest dose of these antagonists in dual combinations or in triple combination. Two additional groups were sedated with an overdose of xylazine (11 mg/kg, IM). At recumbency, 1 of these groups was given saline solution IV and the other group was given yohimbine IV (0.4 mg/kg) as the antagonist. With the 2.2 mg/kg dose of xylazine, control mean arousal time (MAT) and mean walk time (MWT) were 15.5 minutes and 24.8 minutes, respectively. These values were decreased by the individual antagonists to 0.5 to 2.5 minutes and 0.9 to 7.4 minutes, respectively. Approximate equipotent doses of antagonists (mg/kg) were: yohimbine, 0.2; 4-AP, 0.6; and doxapram, 0.5. Relapses did not occur after yohimbine or 4-AP. With doxapram, muscle tremors and spasms, abnormal postures, or aggressive behavior occurred in several dogs and several dogs had partial or complete relapses. The small doses of individual antagonists were synergistic with regard to MAT, MWT, and duration of residual sedation, but the various combinations of antagonists were not more effective in these regards than were larger doses of the single antagonists. With the overdose of xylazine, control MAT and MWT were 41.5 minutes and 144.5 minutes, respectively. Yohimbine decreased these values to 2.2 minutes and 2.5 minutes, respectively. Relapses did not occur.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of tolazoline as an antagonist to xylazine-ketamine-induced immobilization in African elephants

A group of 15 African elephants (Loxodonta africana) were immobilized with a combination of xylazine (0.2 mg/kg of body weight, IM) and ketamine (1 to 1.5 mg/kg of body weight, IM). Ten of the African elephants were allowed to remain recumbent for 30 minutes and the remaining 5 elephants, for 45 minutes before they were given tolazoline (0.5 mg/kg of body weight, IV). For the group of 15, the mean induction time (the time required from injection of the xylazine-ketamine combination until onset of recumbency) was 14.2 +/- 4.35 minutes (mean +/- SD), and standing time (the time required from the tolazoline injection until the elephant stood without stimulation or assistance) was 2.8 +/- 0.68 minutes. All of the elephants were physically stimulated (by pushing, slapping, shouting) before they were given tolazoline, and none could be aroused. After tolazoline was given and the elephant was aroused, relapses to recumbency did not occur. Recovery was characterized by mild somnolence in an otherwise alert and responsive animal. Failure (no arousal) rates were 0% (95% confidence interval, 0 to 0.3085) for elephants given tolazoline after 30 minutes of recumbency and 100% for elephants that were not given tolazoline. There was no significant (P less than 0.05) difference in standing time 30 or 45 minutes after tolazoline injection.     

Evaluation of intramuscular anesthetic protocols in healthy domestic horses

ObjectiveTo assess anesthetic induction, recovery quality and cardiopulmonary variables after intramuscular (IM) injection of three drug combinations for immobilization of horses.Study designRandomized, blinded, three-way crossover prospective design.AnimalsA total of eight healthy adult horses weighing 470–575 kg.MethodsHorses were administered three treatments IM separated by ≥1 week. Combinations were tiletamine–zolazepam (1.2 mg kg⁻¹), ketamine (1 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment TKD); ketamine (3 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment KD); and tiletamine–zolazepam (2.4 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment TD). Parametric data were analyzed using mixed model linear regression. Nonparametric data were compared using Skillings–Mack test. A p value <0.05 was considered statistically significant.ResultsAll horses in treatment TD became recumbent. In treatments KD and TKD, one horse remained standing. PaO₂ 15 minutes after recumbency was significantly lower in treatments TD (p < 0.0005) and TKD (p = 0.001) than in treatment KD. Times to first movement (25 ± 15 minutes) and sternal recumbency (55 ± 11 minutes) in treatment KD were faster than in treatments TD (57 ± 17 and 76 ± 19 minutes; p < 0.0005, p = 0.001) and TKD (45 ± 18 and 73 ± 31 minutes; p = 0.005, p = 0.021). There were no differences in induction quality, muscle relaxation score, number of attempts to stand or recovery quality.Conclusions and clinical relevanceIn domestic horses, IM injections of tiletamine–zolazepam–detomidine resulted in more reliable recumbency with a longer duration when compared with ketamine–detomidine and tiletamine–zolazepam–ketamine–detomidine. Recoveries were comparable among protocols.     

Yohimbine increases plasma insulin concentrations and reverses xylazine-induced hypoinsulinemia in dogs

Xylazine (1.1 mg/kg of body weight, IV), an alpha 2-adrenoreceptor agonist, suppressed the increase in plasma insulin concentration induced by glucose (0.6 g/kg, IV) in dogs. Yohimbine (0.11 mg/kg, IV), an alpha 2-adrenoreceptor antagonist, given 5 minutes after xylazine, reversed effects of xylazine, whereas yohimbine alone increased plasma insulin and decreased plasma glucose concentrations. Seemingly, alpha 2-adrenoreceptors exert a negative control of insulin release.     

Epidural administration of tiletamine/zolazepam in horses

Objectives To evaluate the analgesic, physiologic, and behavioral effects of the epidural administration of tiletamine/zolazepam in horses. Study design Prospective, double‐blind, randomized experimental study. Animals Five adult, healthy horses aged 10–16 years and weighing (mean ± SD) 400 ± 98 kg. Methods The horses were sedated with 1.0 mg kg^?1 intravenous (IV) xylazine, and an epidural catheter was placed into the first intercoccygeal intervertebral space. After a 48‐hour resting period, epidural tiletamine/zolazepam, 0.5 mg kg^?1 (treatment I) or 1.0 mg kg^?1 (treatment II), diluted up to 5 mL in sterile water, was administered with a 1‐week interval between the treatments. Heart rate, respiratory rate, arterial blood pressure, and sedation were evaluated. In order to evaluate the respiratory effects, blood from the carotid artery was withdrawn at time 0 (baseline), and then after 60 and 240 minutes. Analgesia was evaluated by applying a noxious stimulus with blunt‐tipped forceps on the perineal region, and graded as complete, moderate, or absent. Data were collected before tiletamine/zolazepam administration and at 15‐minute intervals for 120 minutes, and 4 hours after tiletamine/zolazepam administration. Data were analyzed with anova and Bonferroni's test with p < 0.05. Results The results showed no significant difference between treatments in cardiovascular and respiratory measurements. Sedation was observed with both doses, and it was significantly different from baseline at 60, 75, and 90 minutes in treatment II. Moderate analgesia and locomotor ataxia were observed with both the treatments. Conclusions and clinical relevance The results suggest that caudal epidural 0.5 and 1.0 mg kg^?1 tiletamine/zolazepam increases the threshold to pressure stimulation in the perineal region in horses. The use of epidural tiletamine/zolazepam could be indicated for short‐term moderate epidural analgesia. There are no studies examining spinal toxicity of Telazol, and further studies are necessary before recommending clinical use of this technique.     

Antagonism of xylazine sedation by 4-aminopyridine and yohimbine in cattle

Twenty-four crossbred steers (4 groups of 6 steers each) were injected IM with a standard dosage range of xylazine hydrochloride (0.2 to 0.3 mg/kg of body weight). When the steers were maximally sedated, group I (control group) were given isotonic saline solution (1 ml, IV), group II were given 4-aminopyridine (4-AP, 0.3 mg/kg) IV, group III were given yohimbine hydrochloride (0.125 mg/kg) IV, and group IV were given 4-AP (0.3 mg/kg) plus yohimbine hydrochloride (0.125 mg/kg) IV. The 4-AP decreased mean standing time (MST; time until animal could stand unaided) from 94.3 minutes (control) to 13.4 minutes. Yohimbine decreased MST to 27 minutes. The combination of 4-AP + yohimbine decreased MST to 7.4 minutes. Mean total recovery time (MTRT; time from xylazine injection until normal behavior, including eating and drinking) was not significantly (P = greater than 0.05) decreased from control values by any of the antagonists tested. The combination of 4-AP + yohimbine decreased MST in animals given a 3X overdose of xylazine (0.6 mg/kg) from 124 minutes (control) to 30.3 min. The MTRT was not significantly (P greater than 0.05) decreased from control values. Two animals given a 5X overdose of xylazine (1 mg/kg) and then given 4-AP + yohimbine had a MST of 32.5 minutes and a MTRT of 3.7 hours. The combination of 4-AP + yohimbine produced marked antagonism of xylazine sedation in cattle. The combination of antagonists may prove to be useful for the arousal of animals sedated with xylazine alone or with a combination of sedatives including xylazine.     

Effect of yohimbine on xylazine-induced immobilization in white-tailed deer

Two groups of white-tailed deer were given IM injections of xylazine with a projectile syringe. Deer in one of the groups served as controls and did not receive any treatments other than xylazine. Deer in the other group were given yohimbine IV at various times (15 to 171 minutes) to evaluate its effect on xylazine-induced immobilization. In 5 control deer given 3.7 +/- 1.2 mg of xylazine/kg (mean +/- SD), onset of recumbency was 13 +/- 2 minutes and time to standing was 268 +/- 76 minutes. In 20 principal deer given 2.8 +/- 1.0 mg of xylazine/kg, onset of recumbency was 8 +/- 7 minutes, time to sitting after giving yohimbine was 3 +/- 4 minutes in 18 of the deer, and time to standing after giving yohimbine was 4 +/- 5 minutes in 19 of the deer. Most of these deer were still moderately sedated 30 minutes after injection of yohimbine, but none of them became reimmobilized or as deeply sedated as before the injection of yohimbine. Yohimbine also reversed the bradycardia and respiratory depression induced by xylazine.     

Effects of xylazine and/or butorphanol or neostigmine on myoelectric activity of the cecum and right ventral colon in female ponies

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less than 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.     

Effect of xylazine on heart rate and arterial blood pressure in conscious dogs, as influenced by atropine, 4-aminopyridine, doxapram, and yohimbine

The effects of xylazine on heart rate (HR) and mean arterial blood pressure (ABP) were studied in 5 conscious male dogs. An IV injection of xylazine (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia. Xylazine administration also caused an initial increase in ABP, which was followed by a decrease. Atropine sulfate (0.045 mg/kg, IM) increased both the ABP and HR, but prevented xylazine-induced bradycardia only in 3 of 5 dogs. The other 2 dogs had to be given a supplemental dose of atropine sulfate (0.01 mg/kg, IV) before xylazine-induced bradycardia was antagonized. In addition, atropine sulfate potentiated xylazine-induced hypertension for 60 minutes. Yohimbine, an alpha 2-adrenoreceptor blocking agent, given IV at a dosage of 0.1 mg/kg, antagonized hypertension, hypotension, and bradycardia induced by xylazine. In addition, doxapram HCl, given IV at a dosage of 5.5 mg/kg, antagonized bradycardia but potentiated xylazine-induced hypertension, and an IV injection of 4-aminopyridine at a dosage of 0.5 mg/kg did not affect the cardiovascular actions of xylazine. It was concluded that atropine sulfate at the IM dosage of 0.045 mg/kg may be insufficient to antagonize xylazine-induced bradycardia but may potentiate xylazine-induced hypertension, and yohimbine may be useful in antagonizing these untoward reactions associated with xylazine administration. Doxapram and 4-aminopyridine were not found to be beneficial.