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.     

Cardiovascular effects of xylazine recorded with telemetry in the dog

Cardiovascular effects of xylazine have not been studied with telemetry in dogs. In the present study, the effects on cardiovascular parameters after intramuscular (i.m.) administration of 2.0 mg/kg xylazine were studied via telemetry in unrestrained dogs. Telemetry transmitters were implanted subcutaneously (s.c.) with a pressure catheter in the femoral artery. Cardiovascular effects and body temperature effects were assessed after i.m. administration of xylazine. Heart rate decreased for about 10 min and was continuously depressed during 60 min. Thereafter, heart rate slowly increased but had not fully reached pre-dose values 4 h after treatment. Both systolic and diastolic blood pressure increased immediately after administration of xylazine. The systolic blood pressure showed a peak increase for about 5-10 min and then decreased below the baseline value not normalizing within 90 min. The diastolic blood pressure peaked 5-10 min after xylazine administration but did not return to baseline level until 50 min after administration. Body temperature decreased continuously for about 90 min and remained low for more than 4 h after treatment. An additional administration of xylazine to the same individuals after a recovery period of 4 weeks induced exactly the same response in systolic and diastolic blood pressure and in heart rate. By using the telemetric recording system it was possible to continuously evaluate xylazine-induced cardiovascular responses in a way that is not possible with conventional techniques.     

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.     

Ultrasonographic evaluation of reticular motility in cows after administration of atropine,scopolamine and xylazine

The goal of this study was to evaluate the effect of various dosages and routes of administration of atropine, scopolamine and xylazine on reticular motility in cows. Groups of five cows received atropine, scopolamine or xylazine at dosages varying from 0.01 to 0.20 mg/kg. The drugs were administered intramuscularly and intravenously; atropine was also given subcutaneously. A total of 17 trials, each using five cows, were carried out. Reticular motility was assessed for 3 min immediately prior to the administration of a drug and for 21 min after administration, and the latter period was divided into seven 3-min intervals. The motility was further assessed during 3-min periods every 10 min starting 28 min and ending 141 min after administration of a drug. During each 3-min interval, the number of reticular contractions or the occurrence of reticular atony was determined. Onset and duration of reticular atony were assessed. All three drugs inhibited reticular motility but onset varied with route of administration and dosage. As expected, the onset of reticular atony occurred most rapidly after intravenous administration of each drug, followed by intramuscular and subcutaneous administration. Reticular atony occurred 0-3.0 min after the intravenous administration of each drug and at all dosages except the lowest dosage of atropine. Atony lasted for 3-111 min. Reticular atony occurred 3-18 min and 9-15 min after intramuscular and subcutaneous administration, respectively. It lasted 32-108 min and 39-122 min for the intramuscular and subcutaneous routes, respectively. For each drug, higher dosages resulted in a more rapid onset and longer duration of reticular atony than did lower dosages. This study demonstrated that administration of atropine, scopolamine and xylazine results in reticular atony. Whether this has clinical relevance requires further investigation.     

Cardiovascular and haemodynamic effects of intramuscular doses of xylazine in conscious sheep

OBJECTIVE: To determine if a commonly used analgesic dose of xylazine has detrimental cardiovascular or haemodynamic effects in sheep. DESIGN: A physiological study following intramuscular administration of xylazine. PROCEDURE: Xylazine (50 micrograms/kg) was injected intramuscularly into six healthy Merino ewes. For 60 min heart rate, mean arterial blood pressure and cardiac output were recorded; arterial blood samples for the measurement of blood gas tensions were also collected. RESULTS: There were no significant changes in heart rate, mean arterial blood pressure, cardiac output or arterial carbon dioxide tension. A slight degree of arterial hypoxaemia was noted with a 10% reduction in arterial oxygen tension values at 30 min. CONCLUSION: The minimal changes to cardiovascular and respiratory values in this study verify the safety of previously suggested analgesic dosing regimens for sheep. Previously reported hypoxaemic effects in sheep as a result of intravenous xylazine administration appear to be reduced as a result of intramuscular administration.     

Effects of atropine,scopolamine and xylazine on the placement of an orally administered magnet in cows

This study was carried out to determine whether the administration of atropine, scopolamine or xylazine to cows before the administration of a magnet orally would help to position it in the reticulum. The transit time of the magnet through the oesophagus was also measured. Sixty Swiss Braunvieh cows were examined by radiography and ultrasonography to locate the reticulum. They were then divided into six groups of 10. Before the administration of the magnet, a control group received 4 ml saline solution subcutaneously, one group received 0.10 mg/kg of atropine subcutaneously, a second received 0.05 mg/kg of atropine intravenously, a third received 0.15 mg/kg of scopolamine intravenously, a fourth group received 0.02 mg/kg of xylazine intravenously, and the cows in the fifth group were positioned so that their forelimbs were 30 cm lower than their hindlimbs during the administration of the magnet. The passage of the magnet through the oesophagus was timed with a stopwatch and monitored with a compass. In the control group the magnet passed through in less than 60 seconds, but in four of the cows receiving either atropine or xylazine intravenously, or having their forelimbs positioned lower than their hindlimbs, it took longer than 60 seconds. In the cows receiving atropine subcutaneously or scopolamine intravenously, it took the same time as in the control group. All the cows were radiographed one-and-a-half hours after the administration of the magnet to determine its location. In seven of the 10 cows in the control group, the magnet was located in the reticulum, but in the other three it was in the cranial dorsal blind sac of the rumen. In the other five groups the magnet was located in the reticulum of between four and seven of the 10 cows, but in the cranial dorsal sac of the rumen, the rumen or in other sites in the other cows.     

Effects of atropine, acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog

Gastroesophageal sphincter (GES) pressure was 47.9 +/- 1.2 mm of Hg in nontreated dogs. Treatment with atropine, acepromazine, and xylazine reduced GES pressure to 13.2 +/- 2.03, 18.6 +/- 2.14, and 11.7 +/- 1.19 mm of Hg, respectively. Treatment with meperidine resulted in phasic contractions with minimum and maximum pressures of 27.9 +/- 4.55 and 98.9 +/- 9.16 mm of Hg, respectively. Drugs used in anesthetic procedures can reduce GES pressure in dogs.     

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.     

Renal actions of the alpha2-adrenoceptor agonist, xylazine, in the anaesthetised rat

AIMS: The aims of the present study were to characterise the renal effects of the alpha2-adrenergic agonist, xylazine, in the rat and to test the role of changes in glomerular filtration rate, glucosuria, and arginine vasopressin (AVP) in its mechanism of action. METHODS: Male Wistar rats were anaesthetised with pentobarbitone sodium (50 mg/kg), and polyethylene cannulae were surgically placed for blood pressure measurement and for blood and urine collection. Rats were given xylazine and other alpha2 agonists by bolus intravenous dose, and the effects of the drugs were monitored in the presence and absence of the selective alpha2 antagonist, yohimbine, the alpha1, alpha2B antagonist, prazosin, and the V2-receptor antagonist, d(CH2)5 [D-Ile2,Ile4,Ala-NH29]AVP. RESULTS: Xylazine at 2.5 mg/kg caused a significant and prolonged dose-dependent increase in urine flow rate and sodium excretion but had only short-lasting effects on blood pressure, heart rate, and glomerular filtration rate. Prazosin had no effect on the measured responses. Although plasma glucose concentration and glucose excretion rate were increased by xylazine, the magnitudes of these increases were insufficient to account for the diuresis observed. Xylazine, and 2 other alpha2 agonists, clonidine and oxymetazoline, increased urine flow and/or sodium excretion despite the presence of d(CH2)5 [D-Ile2,Ile4,Ala-NH29]AVP. CONCLUSIONS: Xylazine causes a diuretic and natriuretic alpha2A-adrenergic response in the rat that is independent of changes in glomerular filtration rate, the development of glucosuria, or AVP action on the distal nephron of the kidney. CLINICAL RELEVANCE: The adverse effects of xylazine on salt and water balance need to be considered and possibly compensated for by fluid replacement or post-surgical administration of alpha2-receptor antagonists.     

Observations on some cardiopulmonary effects of midazolam, xylazine and a midazolam/ketamine combination in the goat

Xylazine, midazolam and a midazolam/ketamine combination were administered to 6 goats in a randomised 3-way block design. All goats received all treatments with at least a 7-day interval between treatments. Statistically significant (P < 0.05) changes were observed in some of the measured cardiopulmonary variables for xylazine and midazolam/ ketamine. Xylazine administration resulted in statistically significant decreases in minute volume, arterial partial pressure of oxygen, heart rate and mean arterial blood pressure. The increase in arterial partial pressure of carbon dioxide was not statistically significant. For the midazolam/ketamine combination, the decrease in tidal volume was statistically significant, but not the decrease in minute volume and increase in arterial partial pressure of carbon dioxide. The decrease in the arterial partial pressure of oxygen was also statistically significant. The mean arterial blood pressure for the combination was statistically significantly higher compared to xylazine. The changes in cardiopulmonary variables after midazolam administration were not statistically significant, such as tidal and minute volume, arterial partial pressure of oxygen and carbon dioxide. However, clinically significant effects such as hypoventilation and hypoxia were observed after its administration. The change in mean arterial blood pressure was minimal.     

Cardiovascular and pulmonary effects of atropine reversal of oxymorphone-induced bradycardia in dogs.

Oxymorphone was administered intravenously (IV) to 10 dogs (0.4 mg/kg initial dose followed by 0.2 mg/kg three times at 20-minute intervals). Four hours after the last dose of oxymorphone, heart rates were less than 60 bpm in six dogs. After atropine (0.01 mg/kg IV) was administered, heart rate decreased in five dogs and sinus arrhythmia or second degree heart block occurred in four of them. A second injection of atropine (0.01 mg/kg IV) was administered 5 minutes after the first and the heart rates increased to more than 100 bpm in all six dogs. Ten minutes after the second dose of atropine, heart rate, cardiac output, left ventricular minute work, venous admixture, and oxygen transport were significantly increased, whereas stroke volume, central venous pressure, systemic vascular resistance, and oxygen extraction ratio were significantly decreased from pre-atropine values. The PaCO2 increased and the PaO2 decreased but not significantly. The oxymorphone-induced bradycardia did not produce any overtly detrimental effects in these healthy dogs. Atropine reversed the bradycardia and improved measured cardiovascular parameters.     

Comparative analgesia of xylazine, xylazine/morphine, xylazine/butorphanol, and xylazine/nalbuphine in the horse, using dental dolorimetry

Xylazine, morphine, butorphanol, and nalbuphine were evaluated in 5 adult male horses, using dental dolorimetry. Comparisons were made at 30, 60, and 100 minutes after IV drug administration. Peak analgesia and the time to develop peak analgesia also were compared. Xylazine induced a marked increase in the tooth pulp pain threshold measurements as did the xylazine/narcotic combinations. Statistical differences were not detectable between these treatments. Xylazine and xylazine/butorphanol were better analgesics than was butorphanol alone at 30 and 60 minutes. Xylazine resulted in peak analgesia faster than did butorphanol or the combination of xylazine/butorphanol. Additive analgesic effects were not detected with the combined treatments.     

Probable post-synaptic α2 adrenergic mediated effect of xylazine on goat uterine motility*

Perez, R., Cox, J.F., Arrue, R. Probable post-synaptic ot2 adrenergic mediated effect of xylazine on goat uterine motility. J. vet. Pharmacol. Therap. 17 , 59–63. Xylazine has been characterized as a selective α₂-adrenoceptor agonist, which has explained its central nervous system depressant and other pharmacological effects. In order to characterize the effect of xylazine on uterine motility during the oestrus cycle in goats intrauterine pressure changes were recorded in cycling goats using balloon-tipped catheters placed in the uterine horns and connected to pressure transducers and a recorder. The effect of xylazine on myometrial activity was studied by giving increasing doses of the drug (1.0, 10.0, 100.0 or 500.0 m̈g/kg) intravenously (i.v.) to animals either in the follicular or the luteal phase of the cycle. To establish the subtype of a adrenergic receptor mediating the action of xylazine, goats were pretreated with either prazosin (1.0 mg/kg, i.v.) or yohimbine (1.0 m̈g/kg, i.v.). To establish whether the effect of xylazine was pre- or post-synaptic, xylazine (100 mg/kg, i.v.) was administered to goats pretreated with reserpine (0.8 mg/kg, i.p.) to deplete presynaptic catecholamine stores. Xylazine induced a significant and dose-dependent increase on uterine motility in cycling goats, apparently mediated by postsynaptic oc₂-adrenoceptors.     

Cardiovascular and autonomic nervous effects of edrophonium and atropine combinations during neuromuscular blockade antagonism in sheep

ObjectiveTo study heart rate (HR), arterial blood pressure (BP) and autonomic nervous (AN) effects of edrophonium–atropine combinations during neuromuscular blockade (NMB) antagonism in sheep.Experimental design Randomized, prospective and experimental study.AnimalsSeventy-eight Scottish blackface ewes; mean age: 4.5 years; mean body mass: 54 kg.MethodsAfter induction with IV etomidate (0.5 mg kg⁻¹) and midazolam (0.5 mg kg⁻¹), anaesthesia was maintained with halothane and NMB produced with atracurium or mivacurium. In the first study (n = 53), the electrocardiographic (ECG), HR, BP and AN effects of low (40 μg kg⁻¹) and high (80 μg kg⁻¹) atropine doses combined with either of two edrophonium doses (0.5 or 1.0 mg kg⁻¹) were investigated. These variables were also measured in a second study when edrophonium (1.0 mg kg⁻¹) was administered 5 minutes before atropine (80 μg kg⁻¹) and vice versa. Data were analysed using one-way within-subjects and repeated measures anova.ResultsIn the first study, all combinations reversed NMB but significantly (p < 0.001) increased HR and BP within 2 minutes without arrhythmias. In the second study, edrophonium (1.0 mg kg⁻¹) significantly increased HR and BP, saliva flow (n = 1) and lung sounds (n = 3) and caused ECG changes (n = 1). Cardiovascular changes were partially reversed by atropine (80 μg kg⁻¹) administered 5 minutes later. Administered first, atropine (80 μg kg⁻¹) significantly decreased HR and BP effects which were fully (HR) and partially (BP) reversed by edrophonium (1 mg kg⁻¹) administered 5 minutes later.Conclusion and clinical relevance The cardiovascular effects of edrophonium and atropine were opposite to those reported in humans and dogs. Edrophonium (0.5 mg kg⁻¹) and atropine (80 μg kg⁻¹) caused the mildest HR changes without ECG and noncardiac AN disturbances, and is recommended for the antagonism of NMB in sheep.     

Cardiovascular effects of a continuous rate infusion of lidocaine in calves anesthetized with xylazine,midazolam, ketamine and isoflurane

ObjectiveTo assess the cardiovascular changes of a continuous rate infusion of lidocaine in calves anesthetized with xylazine, midazolam, ketamine and isoflurane during mechanical ventilation.Study designProspective, randomized, cross-over, experimental trial.AnimalsA total of eight, healthy, male Holstein calves, aged 10 ± 1 months and weighing 114 ± 11 kg were included in the study.MethodsCalves were administered xylazine followed by ketamine and midazolam, orotracheal intubation and maintenance on isoflurane (1.3%) using mechanical ventilation. Forty minutes after induction, lidocaine (2 mg kg^?1 bolus) or an equivalent volume of saline (0.9%) was administered IV followed by a continuous rate infusion (100 μg kg^?1 minute^?1) of lidocaine (treatment L) or saline (treatment C). Heart rate (HR), systolic, diastolic and mean arterial pressures (SAP, DAP and MAP), central venous pressure (CVP), mean pulmonary arterial pressure (mPAP), pulmonary arterial occlusion pressure (PAOP), cardiac output, end-tidal carbon dioxide (Pe’CO₂) and core temperature (CT) were recorded before lidocaine or saline administration (Baseline) and at 20-minute intervals (T20-T80). Plasma concentrations of lidocaine were measured in treatment L.ResultsThe HR was significantly lower in treatment L compared with treatment C. There was no difference between the treatments with regards to SAP, DAP, MAP and SVRI. CI was significantly lower at T60 in treatment L when compared with treatment C. PAOP and CVP increased significantly at all times compared with Baseline in treatment L. There was no significant difference between times within each treatment and between treatments with regards to other measured variables. Plasma concentrations of lidocaine ranged from 1.85 to 2.06 μg mL^?1 during the CRI.Conclusion and clinical relevanceAt the studied rate, lidocaine causes a decrease in heart rate which is unlikely to be of clinical significance in healthy animals, but could be a concern in compromised animals.     

The effect of xylazine and xylazine followed by insulin on blood glucose and insulin in the dairy cow

The effect of xylazine and xylazine followed 20 minutes later by insulin upon glucose metabolism and plasma insulin concentrations was examined in three cows. After doses of 0.18 mg per kg xylazine given intramuscularly (IM) or 0.15 mg per kg given intravenously (IV) hepatic glucose production increased, plasma insulin concentrations decreased to 25 to 33 per cent of control values, and there was a prolonged hyperglycaemia. When 200 units of soluble insulin were given 20 minutes after similar doses of xylazine there was a rapid fall in blood glucose and a reduction in the rate of glucose production by the liver. Xylazine-induced hyperglycaemia arose from a combination of increased hepatic glucose production and reduced plasma insulin concentrations. Peripheral tissues were still responsive to insulin and when adequate insulin was available blood glucose concentrations rapidly decreased.     

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)