Effect of adrenergic drugs on glucose and plasma glucagon and insulin responses to xylazine in sheep

Xylazine was administered intravenously (0.16 mg/kg) to sheep. This was associated with a transient hyperglucagonaemia, hypoinsulinaemia and hyperglycaemia. The rate of glucose appearance as determined by isotope dilution techniques was increased three to four fold during the first 20 minutes after xylazine administration. Phentolamine prevented the xylazine-induced increase in the rate of appearance of glucose, and in concentrations of glucose and glucagon in plasma. The insulin response was not altered by phentolamine. Propranolol had no effect on the glucose and hormonal responses due to xylazine. The xylazine-induced effects on glucose metabolism and secretion by glucagon and insulin appear to be mediated by the alpha-adrenoceptors.     

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.     

Effect of yohimbine on xylazine-induced hypoinsulinemia and hyperglycemia in mares

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.     

Effects of intravenous xylazine hydrochloride on blood glucose, plasma insulin and rectal temperature in neonatal foals

The effects of intravenous xylazine hydrochloride on blood glucose, plasma insulin and rectal temperature were investigated in six foals at 10 and 28 days of age. These variables were also measured in three foals at 19 days of age when saline alone was injected. Rectal temperature fell significantly after 30 mins in both groups of xylazine treated foals and was still depressed after 120 mins. Hypothermia did not occur in the saline control group. There was no significant change in blood glucose or plasma insulin concentrations during the 120 mins following either xylazine or saline administration and no significant differences between the three groups of foals. When foals were allowed to suckle after being away from their dams for 2 h, there was a significant (P less than 0.01) rise in plasma insulin levels in all the groups. Blood glucose showed a concomitant rise but this was only significant in the saline group. Unlike adults, intravenous xylazine (1.1 mg/kg) does not produce hypoinsulinaemia and hyperglycaemia in foals. This study suggests that the inhibition of insulin release from pancreatic beta-cells by xylazine, which in adults is alpha 2-adrenoceptor mediated, is immature or absent in foals under one month of age.     

Effects of xylazine on the stress response to transport in male goats.

A 20-min van journey increased plasma cortisol concentrations to 15-25 ng/ml in male goats, blood glucose concentrations were not affected, but respiratory rates and heart rates were increased, the latter by 40 beats per min. A 2-h van journey increased plasma cortisol to greater than 25 ng/ml and blood glucose to greater than 5 mmol/l. Respiratory rates were increased to greater than 40 breaths per min and heart rates by greater than 100 beats per min. Xylazine alone (0.01 mg/kg) suppressed resting plasma cortisol concentrations, increased blood glucose concentrations to 4.5 +/- 0.8 mmol/l and suppressed respiratory rates by 5-10 breaths per min and heart rates by 20 beats per min. Cortisol concentrations were suppressed by xylazine treatment if given before a 20-min van journey, and for approximately 60 min if given 20 min after the start of a 2-h journey. When combined with transport, xylazine caused an additive effect on glucose concentrations, but suppressed respiratory and heart rates. However, for the latter criteria the timing of suppression was different depending on the time of onset and duration of the stressor. Injection of 50 micrograms ovine corticotrophin releasing factor (CRF) caused an immediate elevation of cortisol concentrations (but not glucose) which lasted for at least 6 h compared with the return to baseline within 60 min after either length of journey. Xylazine pretreatment did not alter the cortisol response to CRF, suggesting that xylazine must act centrally above pituitary level when blocking the cortisol response to transport. It is proposed that under resting conditions the hypothalamus is under alpha 2-adrenergic suppression. Stimulation of cortisol secretion in response to a stressor can be inhibited by an alpha 2-adrenergic agonist.     

Hyperglycaemic effect of xylazine

In cats, xylazine, an analogue of clonidine, produced hyperglycaemia when injected intravenously. The effect was obtained in unanaesthetized cats and in pentobarbitone sodium anaesthesia. The hyperglycaemia was not a central effect, nor due to adrenaline release from the adrenals, nor to a direct action of xylazine on the liver. It resulted from a fall in plasma insulin produced by an action of xylazine on the pancreas, inhibiting insulin secretion without affecting glucagon secretion. The increase in the glucagon/insulin ratio, by stimulating glucose production in the liver, was probably responsible for the xylazine-induced hyperglycaemia.     

Effects of xylazine on renal function and plasma glucose in ponies

The intravenous administration of xylazine (1.1 mg/kg bodyweight) in six ponies resulted in a significant increase in urine output over two hours, with maximum flow occurring between 30 and 60 minutes after injection. Urine specific gravity, osmolality and glucose concentration decreased. Renal clearance of endogenous creatinine was unchanged. Significant increases in the excretion of potassium and chloride occurred. Plasma glucose concentration was increased 30 minutes after the administration of xylazine by a mean value of 37 per cent. Serum osmolality and sodium, potassium and chloride concentrations remained unchanged.     

Evaluation of xylazine as a sedative and preanesthetic agent in horses.

Xylazine administered intramuscularly (IM) to horses at the dose level of 2 mg/kg was an effective sedative and preanesthetic for thiamylal sodium narcosis or thiamylal sodium and halothane anesthesia. Evaluation of response of cardiovascular, respiratory, and hepatic function did not indicate serious untoward effects, although cardiac and respiratory rate decreased, calculated vigor of left ventricular contraction decreased, calculated peripheral vascular resistance increased, and transient innocuous cardiac arrhythmias occurred. Effects of the anesthetics used on respiratory function (blood gases and pH), using xylazine as a preanesthetic, were comparable with those observed when promazine was used. The onset of action of xylazine given IM was at least as rapid as that occurring when promazine was given intravenously; e.g., 5 minutes for first observable effects, and 15 to 20 minutes for maximal effect. Recovery, times from anesthesia when using xylazine administered IM as a preanesthetic agent were comparable with those reported after promazine was given intravenously; moreover, horses given xylazine were more calm during recovery and seldom tried to stand before they were able.     

Cardiopulmonary and sedative effects of intravenous administration of low doses of medetomidine and xylazine to adult horses

OBJECTIVE: To determine the cardiopulmonary and sedative effects of medetomidine hydrochloride in adult horses and to compare those effects with effects of an equipotent dose of xylazine hydrochloride. ANIMALS: 10 healthy adult female horses. PROCEDURE: 5 horses were given medetomidine (4 microg/kg of body weight, i.v.), and the other 5 were given xylazine (0.4 mg/kg, i.v.). Heart rate, respiratory rate, arterial blood pressures, pulmonary arterial blood pressures, and cardiac output were recorded, and sedation and ataxia scores were assigned before and every 5 minutes after drug administration for 60 minutes. Rectal temperature and blood gas partial pressures were measured every 15 minutes after drug administration. RESULTS: Arterial blood pressure was significantly decreased throughout the study among horses given medetomidine and was significantly decreased for 40 minutes among horses given xylazine. Compared with baseline values, cardiac output was significantly decreased 10, 20, and 40 minutes after administration of medetomidine and significantly increased 40 and 60 minutes after administration of xylazine. Despite the significant decrease in respiratory rate in both groups, results of blood gas analyses were not significantly changed over time. Ataxia and sedation scores were of similar magnitude for the 2 groups, but ataxia persisted slightly longer among horses given medetomidine. Horses resumed eating hay 10 to 55 minutes after drug administration. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that equipotent low doses of medetomidine and xylazine induce comparable levels of ataxia and sedation and similar cardiopulmonary changes in adult horses.     

Effect of xylazine in heifers under thermoneutral or heat stress conditions

A study was performed to assess the effect of xylazine HCl (0.1 mg/kg of body weight, IV) in heifers maintained at thermoneutrality (18 C, 42% humidity) or under heat stress (33 C, 63% humidity) conditions. Xylazine caused 50 and 70% decreases in serum insulin concentrations in the thermoneutral and heat-stressed heifers, respectively. Xylazine-induced hypoinsulinemia was associated with hyperglycemia. In the thermoneutral group, serum glucose concentrations increased from a basal concentration of 75 mg/dl to 150 mg/dl after 15 minutes. In the heat stress group, the serum glucose concentration increased from 65 mg/dl to 105 mg/dl. Hyperglycemia peaked at 2 hours and remained high for 6 hours after xylazine administration. Heat-stressed heifers took a longer time (107 minutes) to stand than did heifers under thermoneutral conditions (41 minutes). The time to regain sensation to pain was significantly prolonged in heat-stressed heifers. Xylazine had no effect on body temperature and respiration rate in heifers under the thermoneutral condition, whereas it markedly induced hyperthermia and suppressed respiration rate in the heat-stressed heifers. Furthermore, the pulse rate was slightly decreased in thermoneutral heifers and was markedly decreased in the heat-stressed heifers.     

Sedative and cardiopulmonary effects of medetomidine hydrochloride and xylazine hydrochloride and their reversal with atipamezole hydrochloride in calves

OBJECTIVE: To assess the sedative and cardiopulmonary effects of medetomidine and xylazine and their reversal with atipamezole in calves. ANIMALS: 25 calves. PROCEDURES: A 2-phase (7-day interval) study was performed. Sedative characteristics (phase I) and cardiopulmonary effects (phase II) of medetomidine hydrochloride and xylazine hydrochloride administration followed by atipamezole hydrochloride administration were evaluated. In both phases, calves were randomly allocated to receive 1 of 4 treatments IV: medetomidine (0.03 mg/kg) followed by atipamezole (0.1 mg/kg; n = 6), xylazine (0.3 mg/kg) followed by atipamezole (0.04 mg/kg; 7), medetomidine (0.03 mg/kg) followed by saline (0.9% NaCl; 6) solution (10 mL), and xylazine (0.3 mg/kg) followed by saline solution (10 mL; 6). Atipamezole or saline solution was administered 20 minutes after the first injection. Cardiopulmonary variables were recorded at intervals for 35 minutes after medetomidine or xylazine administration. RESULTS: At the doses evaluated, xylazine and medetomidine induced a similar degree of sedation in calves; however, the duration of medetomidine-associated sedation was longer. Compared with pretreatment values, heart rate, cardiac index, and PaO(2) decreased, whereas central venous pressure, PaCO(2), and pulmonary artery pressures increased with medetomidine or xylazine. Systemic arterial blood pressures and vascular resistance increased with medetomidine and decreased with xylazine. Atipamezole reversed the sedative and most of the cardiopulmonary effects of both drugs. CONCLUSIONS AND CLINICAL RELEVANCE: At these doses, xylazine and medetomidine induced similar degrees of sedation and cardiopulmonary depression in calves, although medetomidine administration resulted in increases in systemic arterial blood pressures. Atipamezole effectively reversed medetomidine- and xylazine-associated sedative and cardiopulmonary effects in calves.     

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.     

Reversal of pentobarbital anesthesia with 4-aminopyridine and yohimbine in cats pretreated with acepromazine and xylazine

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).     

Neurohormonal and metabolic effects of medetomidine compared with xylazine in beagle dogs

This study was aimed to investigate and compare the effects of medetomidine and xylazine on the blood level of some stress-related neurohormonal and metabolic variables in clinically normal dogs, especially focusing on time and dose relations of the effects. A total of 9 beagle dogs were used for 9 groups, which were treated with physiological saline solution (control), 10, 20, 40, and 80 μg/kg medetomidine, and 1, 2, 4, and 8 mg/kg xylazine, intramuscularly. Blood samples were taken at 10 times during 24 h from a central venous catheter. Plasma norepinephrine, epinephrine, cortisol, glucose, insulin, glucagon, and non-esterified fatty acid concentrations were determined. Both medetomidine and xylazine similarly and dose-dependently inhibited norepinephrine release and lipolysis. Medetomidine suppressed epinephrine release dose-dependently with greater potency than xylazine. Xylazine also tended to decrease epinephrine levels dose-dependently. The cortisol and glucagon levels did not change significantly in any treatment group. Both drugs suppressed insulin secretion with similar potency. Both medetomidine and xylazine increased glucose levels. The hyperglycemic effect of medetomidine, in contrast with xylazine, was not dose-dependent at the tested dosages. The results suggested that the effect of medetomidine on glucose metabolism may not be due only to α₂-adrenoceptor-mediated actions.     

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)     

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.     

Effects of ketamine, xylazine, and a combination of ketamine and xylazine in Pekin ducks

Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, PaCO2 and PaO2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, PaCO2, and PaO2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and PaO2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Xylazine-induced hyperglycemia in beef cattle.

Intravenous administration of xylazine to beef cattle (10 animals, 0.2 mg/kg of body weight) resulted in rapid onset (less than 15 minutes) of hyperglycemia. Plasma glucose values increased to 195 +/- 15 mg/dl and 305 +/- 10 mg/dl at 15 minutes and 3 hours, respectively. Concomitantly, plasma insulin concentrations dropped from 23 +/- 2 microU/ml before xylazine to 5.8 +/- 0.7 microU/ml and 2.4 +/- 0.3 microU/ml at 15 minutes and 3 hours, respectively. Parallel decreases (20%) were observed for percentage of hemoglobin, red blood cell number, and packed cell volume. Plasma urea nitrogen was significantly (P less than 0.01) incrased within 3 hours of xylazine administration (6.7 +/- 0.9 mg/dl vs 11.4 +/- 0.7 mg/dl). Marked changes in concentrations of plasma-free fatty acids were not observed. Alternative means of anesthesia must be considered in those instances in which biopsy material is to be used for studies of carbohydrate metabolism in vitro.     

The effect of magnesium aspartate, xylazine and morphine on the immobilization-induced increase in the levels of prolactin in turkey plasma

The effect of pre-treating turkey poults (8 weeks old) with magnesium aspartate, xylazine or morphine on the concentration of prolactin (PRL) in plasma was studied in normal birds, and birds stressed with immobilization. Acute immobilization (2 h) without drug treatment increased significantly the PRL concentration in plasma. Pretreatment with magnesium aspartate (405 mg/ml) at intramuscular doses of 100, 200, and 400 mg/bird decreased significantly, in a dose-dependent manner, the PRL plasma concentration when compared with the immobilized birds. Drug treatment without immobilization had no significant effect on PRL concentration. Similar results were obtained with xylazine (20 mg/ml) when given to birds intramuscularly at doses of 5, 10, or 20 mg/bird, 1 h before immobilization. Morphine, at intramuscular doses of 5 or 10 mg/kg, did not affect significantly the prolactin concentration of immobilized turkeys. At a dose of 25 mg/kg, however, it significantly lowered the PRL plasma concentration in immobilized birds. Morphine treatment alone did not influence significantly the basal PRL plasma concentration.     

Neurohormonal and metabolic effects of medetomidine compared with xylazine in healthy cats

The purpose of this study was to investigate and compare the effects of medetomidine and xylazine on some neurohormonal and metabolic variables in healthy cats. Five cats were used repeatedly in each of 11 groups, which were injected intramuscularly with physiological saline solution (control), 20, 40, 80, 160, and 320 microg/kg of medetomidine, and 0.5, 1, 2, 4, and 8 mg/kg of xylazine. Blood samples were taken over 24 h from the jugular vein for determination of plasma glucose, insulin, cortisol, epinephrine, norepinephrine, glucagon, and nonesterified fatty acid concentrations. Both medetomidine and xylazine induced remarkable hyperglycemia that was dose-dependent except for the response to medetomidine from 0 to 3 h. Both agents suppressed epinephrine and norepinephrine release but not in a dose-dependent manner at the tested dosages. Both agents inhibited insulin release and lipolysis, with similar potency, and tended to suppress cortisol release. The glucagon levels did not change significantly in any of the groups. These results suggest that the effects of medetomidine and xylazine on glucose metabolism and catecholamine release may not be due only to the actions mediated by alpha2-adrenoceptors.