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1.
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.  相似文献   

2.
Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, and alpha 2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of CNS, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered IV. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.  相似文献   

3.
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.  相似文献   

4.
The intravenous injection of a standard dose (0.05 mg/kg) of xylazine inhibited reticuloruminal motility in cattle. Pretreatment with adrenoceptor antagonists showing alpha 2-blocking activity, tolazoline (0.5 mg/kg) and yohimbine (0.2 mg/kg), antagonized the xylazine-induced reticuloruminal amotility. Tolazoline was more effective than yohimbine, since an antagonistic effect was not seen at 0.5 mg/kg yohimbine, and yohimbine at 0.2 mg/kg was less effective than tolazoline at 0.5 mg/kg. An adrenoceptor antagonist showing alpha 1-blocking activity, prazosin, did not prevent the inhibition of reticuloruminal motility by xylazine. The xylazine-induced reticuloruminal amotility was also not prevented by either a dopamine receptor antagonist, domperidone, or an opiate receptor antagonist, naloxone. These results suggest that xylazine inhibits bovine reticuloruminal motility through its activation of alpha 2-adrenoceptors, and show that tolazoline can be used as a specific antagonist of xylazine in studies of the alpha-adrenergic influence on reticuloruminal motility in cattle.  相似文献   

5.
The effects of yohimbine (0.125 mg/kg) on cardiopulmonary parameters in six adult, xylazine treated (0.15 mg/kg), laterally recumbent sheep were studied. Following collection of baseline data, xylazine was administered intravenously and data were collected five and fifteen minutes later. At twenty minutes post-xylazine either yohimbine (0.125 mg/kg) or saline was given and further collection of data occurred at 25, 30, 40 and 50 minutes. Xylazine administration resulted in significant (P less than 0.05) respiratory depression, as reflected by a decrease in arterial oxygen partial pressure (PaO2). No significant changes in haemodynamic variables were observed. Yohimbine produced a significant improvement in PaO2 at the 50 minute period and abolished the paradoxical respiratory pattern when present. The results indicated that yohimbine can be used as an antagonist to control the duration of xylazine induced respiratory depression, although the degree of reversal was less than is clinically desirable.  相似文献   

6.
OBJECTIVE: To determine effects of i.v. administered yohimbine on perineal analgesia, cardiovascular and respiratory activity, and head and pelvic limb position in healthy mares following epidural administration of detomidine hydrochloride solution. ANIMALS: 8 healthy mares. PROCEDURE: Each mare received detomidine hydrochloride (0.06 mg/kg of body weight), administered in the caudal epidural space, followed 61 minutes later by yohimbine (0.05 mg/kg; test) or sterile saline (0.9% NaCl) solution (control), administered i.v., in a randomized, crossover study design with > or = 2 weeks between treatments. Analgesia was determined by lack of sensory perception to electrical stimulation of perineal dermatomes and needle-prick stimulation of coccygeal to 15th thoracic dermatomes. Arterial pH, PaCO2, PaO2, heart and respiratory rates, rectal temperature, arterial blood pressure, and cardiac output were determined, and mares were observed for sweating and urination. Mean scores obtained for test and control groups were compared. RESULTS: Intravenously administered yohimbine significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, changes in pelvic limb position, and sweating and diuresis; antagonized detomidine-induced decreases in heart rate and cardiac output; but did not affect detomidine-induced decrease in respiratory rate. CONCLUSIONS AND CLINICAL RELEVANCE: Most effects of epidurally administered detomidine, except bradypnea, were antagonized by yohimbine, suggesting that detomidine may influence respiratory rate by mechanisms other than stimulation of alpha2-adrenoceptors, or that yohimbine induces respiratory depressant effects. Yohimbine may be an effective alpha2-adrenoceptor antagonist for all but respiratory depression following epidural administration of detomidine to mares.  相似文献   

7.
Halothane MAC (the minimum alveolar concentration of halothane to produce anaesthesia in 50% of the animals tested) was determined to be 0.92 ± 0.16 volumes % in eight English Pointer dogs. Alterations in halothane MAC induced by an intravenous bolus of xylazine (1.1 mg/kg) and then tolazoline (5 mg/kg) was determined in each dog following control (halothane MAC) measurement. Following xylazine administration, MAC significantly decreased to 0.57 ± 0.023%. Immediately following determination of the xylazine-halothane MAC value in each dog, tolazoline was administered and the halothane requirement (MAC) was again assessed. Halothane MAC significantly increased to 1.24 ± 0.036%. Tolazoline administration induced immediate arousal in the xylazine-halothane anaesthetized dogs requiring a rapid increase in halothane concentration to maintain anaesthesia. Thus, the administration of tolazoline, an alpha adrenergic antagonist, following xylazine administration significantly increased the anaesthetic requirement (MAC) of halothane. Xylazine, an alpha 2 adrenergic agonist, decreased halothane anaesthetic requirement (MAC) in the eight dogs studied. These results are consistent with the hypotheses that stimulation of central alpha 2 receptors is the mechanism by which xylazine produces sedation and that inhibition of CNS excitatory neurotransmitter release decreases halothane anaesthetic requirement. In contrast, the increase in halothane requirement and arousal from xylazine-halothane anaesthesia that occurred following i.v. tolazoline administration indicates an increase in CNS excitatory neurotransmitter activity.  相似文献   

8.
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.  相似文献   

9.
With the use of a crossover study design, we investigated the respiratory and cardiovascular effects of naloxone administration in eight healthy Rocky Mountain wapiti (Cervus elaphus nelsoni) anesthetized with carfentanil (10 microg/kg i.m.) and xylazine (0.1 mg/kg). Anesthetized animals showed profound hypoxemia with mild hypercapnia, tachycardia, hypertension, and acidosis prior to naloxone administration. After monitoring equipment was placed, animals were administered either naloxone (2 microg/microg carfentanil i.v.) or an equivalent volume of normal saline. Mean values for PaO2, PaCO2, heart rate, and respiratory rate were significantly different between naloxone- and saline-treated groups, but mean blood pressure, hematocrit, and serum electrolyte concentrations were not. Mean PaO2 was 23.0 +/- 4.1 mm Hg prior to administration of naloxone or saline and increased to 50.2 +/- 7.3 mm Hg after naloxone administration. Mean PaO2 of saline-treated animals did not change significantly. Electrocardiograms of three saline-treated animals suggested myocardial hypoxia. Hypoxemia appeared to be caused by respiratory depression, hemodynamic alterations, and lateral recumbency. All but one animal remained anesthetized after naloxone administration. Anesthesia in all animals was reversed in < or = 4 min with naltrexone (100 mg/mg carfentanil i.v. s.c.) and yohimbine (0.1 mg/kg i.v.). One bolus of naloxone improved oxygenation in carfentanil-xylazine-anesthetized wapiti.  相似文献   

10.
Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.  相似文献   

11.
Intramuscular injection of xylazine induced dose-dependent vomiting in cats (ED50 = 0.277 mg/kg); administration of standard dose of xylazine (2 mg/kg, 2 times the 100% emetic dose) induced vomiting in 100% of the cats studied. The xylazine-induced vomiting was antagonized by adrenoceptor antagonists possessing alpha 2-blocking activity, which were yohimbine, tolazoline, and phentolamine. Of these antagonists, yohimbine was the most effective; the maximal antagonistic effect was seen at 1 mg of yohimbine/kg, a dose at which the other drugs had little or no effect. At the doses studied, prazosin and phenoxybenzamine, adrenoceptor antagonists with alpha 1-blocking activity, did not prevent vomiting induced by xylazine. Beta-Adrenoceptor (propranolol), dopamine receptor (domperidone and chlorpromazine), a cholinoceptor (atropine), an opiate receptor (naloxone), and a histamine-receptor (diphenhydramine) antagonists, at the doses studied, did not prevent xylazine-induced vomiting. Pretreatment with 6-hydroxydopamine failed to prevent xylazine-induced vomiting. These results indicated that xylazine-induced vomiting in cats is mediated by alpha 2-adrenoceptors and suggested that the alpha 2-adrenoceptors mediating the vomiting attributable to xylazine may not be presynaptic alpha 2-receptors located on noradrenergic nerve terminals.  相似文献   

12.
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.  相似文献   

13.
In 2 separate experiments, groups of atropinized cats (6 cats/group) were given acepromazine (0.25 mg/kg of body weight) or xylazine (2.2 mg/kg) IM and anesthetized with pentobarbital. The mean dose of pentobarbital was decreased approximately 36% by acepromazine, and approximately 80% by xylazine, compared with published doses. Anesthetized cats were given IV saline solution (control groups) or were given the antagonists 4-aminopyridine (4-AP; 0.5 mg/kg), yohimbine (0.4 mg/kg), or 4-AP + yohimbine (0.5 mg/kg and 0.4 mg/kg, respectively). In acepromazine-treated cats, 4-AP + yohimbine was the most effective antagonist; arousal and walking occurred in an average of 10.4 minutes and 91.7 minutes, respectively. Yohimbine enhanced the antagonistic effects of 4-AP. In xylazine-treated cats, yohimbine was an effective antagonist; arousal and walking occurred in an average of 2.8 minutes and 12.8 minutes, respectively. Yohimbine did not enhance the antagonistic effects of 4-AP. Mean respiratory rates were decreased by acepromazine, but were increased by xylazine. Thus, respiratory rate depression by pentobarbital was not as marked with xylazine as it was with acepromazine. Changes in mean heart rate were not remarkable with either sedative, and cardiac irregularities were not palpated or auscultated. In healthy cats, the duration of pentobarbital anesthesia can be controlled by 4-AP + yohimbine (acepromazine-pretreated cats) or by yohimbine alone (xylazine-pretreated cats).  相似文献   

14.
Twelve adult rhebok (Pelea capreolus) were immobilized using a combination of 0.4 mg/kg xylazine and either 0.01 mg/kg of carfentanil (n = 6) or 0.01 mg/kg etorphine (n = 6), delivered i.m. using a remote injection system. Induction and recovery times, heart rate, respiratory rate, rectal temperature, oxygen saturation, end-tidal CO2 (ETCO2), anesthetic depth, indirect blood pressure, and arterial blood gases were recorded. Rhebok were not intubated but nasal oxygen was administered. Forty minutes after induction, anesthesia was antagonized with naltrexone and yohimbine. Mean initial heart rate was significantly higher in the carfentanil group than in the etorphine group. Mean initial oxygen saturation was consistent with hypoxia in both the carfentanil group and the etorphine group. In both groups, arterial pH decreased and partial pressure of carbon dioxide increased during the first 15 min of anesthesia, and values were similar in both groups. These findings were consistent with respiratory acidosis and decreased ventilation. Values for respiratory rate, temperature, oxygen saturation, ETCO2, and blood pressure were similar for both groups at all time periods. During the first 5 min of anesthesia, rhebok in the carfentanil group were more responsive to stimuli than rhebok in the etorphine group. After administration of antagonists, time to first arousal was significantly shorter in the etorphine group than in the carfentanil group. Although cardiopulmonary values were similar for the two groups, rhebok in the carfentanil group were at a comparatively lighter plane of anesthesia, and some individuals in this group required additional manual and chemical restraint for medical procedures to be performed. In conclusion, for captive adult rhebok, 0.01 mg/kg of etorphine and 0.4 mg/kg of xylazine are recommended over 0.01 mg/kg carfentanil and 0.4 mg/kg xylazine because of qualitatively better anesthetic episodes and shorter recovery times.  相似文献   

15.
Inhibition of the cyclical contractions of the reticulum and the rumen by detomidine (10-40 micrograms/kg, i.v.), xylazine (20-80 micrograms/kg, i.v.) and clonidine (2.5-10 micrograms/kg, i.v.) were compared in sheep and cattle housed individually in box stalls. Two alpha 2-adrenergic receptor blocking agents, tolazoline and yohimbine, were administered intravenously for prevention (0.1-0.4 mg/kg) or reversal (0.4-1.2 mg/kg) of these effects. Continuous recording of the reticuloruminal contractions and measurement of the volume of ruminal gas eliminated through the upper respiratory tract indicated that the three alpha 2-agonists inhibited the primary ruminal contractions associated with the reticular contractions. The occurrence of secondary ruminal contractions was also blocked in sheep, but only suppressed in cattle. The inhibition of reticulo-ruminal contractions was prevented or reversed competitively by the two alpha 2-blocking agents, suggesting an alpha 2-adrenoceptor mediation of the inhibition of cyclical motor activity of the reticulo-rumen. In contrast with tolazoline, yohimbine was unable to alleviate the accumulation of gas resulting from inhibition of the secondary ruminal contractions.  相似文献   

16.
Serum insulin and plasma glucose concentrations were determined in 8 mares. Four IV treatments were studied: xylazine (1.1 mg/kg of body weight); yohimbine (0.125 mg/kg); yohimbine (0.125 mg/kg) followed 5 minutes later by xylazine (1.1 mg/kg); and 5 ml of isotonic saline solution as a control. Blood samples were collected before (time 0) and at 5, 15, 30, 60, 120, and 180 minutes after drug administration. Serum insulin concentration decreased and plasma glucose concentration increased in mares given xylazine. Plasma glucose concentration was unchanged in control mares and in mares given yohimbine or yohimbine followed by xylazine. Serum insulin concentration was unchanged in mares given saline solution, but transiently increased in mares given yohimbine alone. Treatment with yohimbine prevented xylazine-induced hypoinsulinemia and hyperglycemia.  相似文献   

17.
Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, Cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [IV]) followed 20 minutes later by either tolazoline (4.0 mg/kg IV) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes after detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in Cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by Cortisol, glucose, and free fatty acids. If antagonism of an α-agonist is contemplated, the potential effect on hormones and metabolites should be considered.  相似文献   

18.
The ability of the antagonists tolazoline, yohimbine and the combination of yohimbine with 4-aminopyridine to reverse the effects of the xylazine-component of the "Hellabrunn mixture" (125 mg/ml xylazine and 100 mg/ml ketamine) on nondomestic zoo ruminants is discussed. Arousal time, recovery time and changes in the parameter of circulatory and respiratory functions after antagonization are shown. Tolazoline is able to antagonize the xylazine effect completely within a short time. Using a dosage of 3-5 mg/kg there is a marked negative effect on the cardio-vascular system. Yohimbine in the used dosage of 0.25-0.3 mg/kg in non-domestic ruminants did not approve in its effects. Combining yohimbine (0.25-0.3 mg) with 4-aminopyridine (0.5 mg/kg) recovery time is about 30 minutes. The negative effect on the cardio-vascular system is less pronounced compared with tolazoline.  相似文献   

19.
OBJECTIVE: To determine the effects of ketamine hydrochloride, xylazine hydrochloride, and lidocaine hydrochloride after subarachnoid administration in goats. ANIMALS: 6 healthy goats. PROCEDURE: In each goat, ketamine (3 mg/kg), xylazine (0.1 mg/kg), lidocaine (2.5 mg/kg), and saline (0.9% NaCI) solution were injected into the subarachnoid space between the last lumbar vertebra and first sacral vertebra (time 0). Analgesic, ataxic, sedative, cardiovascular, and respiratory effects and rectal temperature were evaluated before (baseline) and 2, 5, 10, 15, and 30 minutes after administration and at 30-minute intervals thereafter as needed. RESULTS: Administration of anesthetics induced varying degrees of analgesia. Onset of the analgesic effect was more delayed for xylazine (mean +/- SD, 9.5 +/- 2.6 minutes) than for ketamine (6.7 +/- 2.6 minutes) or lidocaine (3.5 +/- 1.2 minutes). Duration of analgesia induced by xylazine (88.3 +/- 15 minutes) was twice as long as the duration of analgesia induced by ketamine (48.8 +/- 13.5 minutes) but similar to that induced by lidocaine (66.5 +/- 31 minutes). Xylazine induced bradycardia, whereas ketamine caused a nonsignificant increase in heart rate. Xylazine induced a reduction in arterial pressure, whereas ketamine or lidocaine did not affect arterial pressure. CONCLUSIONS AND CLINICAL RELEVANCE: Subarachnoid administration of xylazine in goats resulted in longer duration of analgesia of the tail, perineum, hind limbs, flanks, and caudodorsal rib areas than administration of ketamine or lidocaine. However, xylazine caused bradycardia and respiratory depression. Additional studies are needed to determine whether the analgesia would be sufficient to allow clinicians to perform surgical procedures.  相似文献   

20.
This study was carried out to determine whether yohimbine antagonizes the retrograde flow of spermatozoa into the urinary bladder of dogs caused by xylazine. Adult dogs were assigned to one of four groups of six dogs each and treated as follows: saline control, xylazine (2.2 mg/kg, i.m.), yohimbine (0.2 mg/kg, im.), yohimbine/xylazine (yohimbine, 0.2 mg/kg, i.m., followed 10 min later by xylazine. 2.2 mg/kg, i.m.). Pre- and post-treatment urine were collected by cystocentesis from all dogs. The mean (± SD) adjusted total number of spermatozoa in the post-treatment urine of xylazine-treated dogs (141.02 ± 136.75 × 106) was 15 times higher ( P < 0.05) than the number in the post-treatment urine of control dogs (9.16 ± 20.26 × 106), 1763 times higher ( P < 0.05) than the number in the urine of yohimbine-treated dogs (0.08 ± 0.20 × 106), and 56 times higher ( P < 0.05) than the total number in the post-treatment urine of yohimbine/xylazine-treated dogs (2.54 ± 4.54 × 106). These results confirm that xylazine induces a significant ( P = 0.007) displacement of spermatozoa into the urinary bladder of dogs and demonstrate that pre-treatment with yohimbine prevents this effect.  相似文献   

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