Effects of atropine on xylazine-pentobarbital anesthesia in dogs: preliminary study

The influence of atropine on anesthesia induced by xylazine-pentobarbital administration was studied in 5 dogs. The combination of xylazine (2.2 mg/kg of body weight, IM) and pentobarbital (14.0 mg/kg, IV) caused anesthesia with the duration of absence of the pedal reflex, duration of anesthesia, and the time from return of consciousness to ambulation to be 107.4, 123.4, and 59.2 minutes, respectively. Bradycardia and short-term respiratory depression were observed. An IM injection of atropine sulfate (0.045 mg/kg) did not significantly change the durations of absence of the pedal reflex and of anesthesia, the time from return of consciousness to ambulation, or the pattern of respiration in the anesthetized dogs. The PaO2 increased gradually in both groups; however, atropine caused a marked tachycardia and increased the PaCO2. Fifteen minutes after pentobarbital injection, administration of atropine sulfate caused a slight but significant (P less than 0.01) decrease in arterial pH. Although atropine sulfate antagonized xylazine bradycardia, the data indicated that it may have caused increased respiratory depression in dogs anesthetized with xylazine and pentobarbital.     

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)     

Effects of xylazine on ventilation in horses.

The effects of 3 commonly used dosages (0.3, 0.5, and 1.1 mg/kg of body weight, IV) of xylazine on ventilatory function were evaluated in 6 Thoroughbred geldings. Altered respiratory patterns developed with all doses of xylazine, and horses had apneic periods lasting 7 to 70 seconds at the 1.1 mg/kg dosage. Respiratory rate, minute volume, and partial pressure of oxygen in arterial blood (PaO2) decreased significantly (P less than 0.001) with time after administration of xylazine, but significant differences were not detected among dosages. After an initial insignificant decrease at 1 minute after injection, tidal volume progressively increased and at 5 minutes after injection, tidal volume was significantly (P less than 0.01) greater than values obtained before injection. Partial pressure of carbon dioxide in arterial blood (PaCO2) was insignificantly increased. After administration of xylazine at a dosage of 1.1 mg/kg, the mean maximal decrease in PaO2 was 28.2 +/- 8.7 mm of Hg and 22.2 +/- 4.9 mm of Hg, measured with and without a respiratory mask, respectively. Similarly, the mean maximal increase in PaCO2 was 4.5 +/- 2.3 mm of Hg and 4.2 +/- 2.4 mm of Hg, measured with and without the respiratory mask, respectively. Significant interaction between use of mask and time was not detected, although the changes in PaO2 were slightly attenuated when horses were not masked. The temporal effects of xylazine on ventilatory function in horses should be considered in selecting a sedative when ventilation is inadequate or when pulmonary function testing is to be performed.     

Effect of xylazine on the arrhythmogenic dose of epinephrine in thiamylal/halothane-anesthetized horses.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration (MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 micrograms/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 micrograms/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 micrograms/kg/min; xylazine, 1.21 +/- 0.46 micrograms/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.     

Cardiorespiratory effects of a tiletamine/zolazepam-ketamine-detomidine combination in horses.

OBJECTIVE: To determine cardiorespiratory effects of a tiletamine/zolazepam-ketamine-detomidine (TZKD) combination in horses. ANIMALS: 8 healthy adult horses. PROCEDURE: Horses were instrumented for measurement of cardiorespiratory, acid-base, and electrolyte values. Each horse was given xylazine (0.44 mg/kg of body weight, IV) 10 to 15 minutes prior to induction of recumbency by administration of the TZKD combination. Cardiorespiratory, acid-base, and electrolyte values were measured at 5-minute intervals for > or =30 minutes. RESULTS: All horses became recumbent within 1 minute after IV administration of TZKD. Mean +/- SD duration of recumbency was 40+/-8 minutes. All horses regained standing position after < or =2 attempts. Quality of anesthesia and analgesia was determined to be satisfactory in all horses. Xylazine induced decreases in respiratory rate, heart rate, cardiac output, maximum rate of increase of right ventricular pressure, and rate pressure product. The PaCO2, right atrial pressure, and peripheral vascular resistance increased, whereas blood temperature, PO2, pHa, HCO3-, PCV, total solids, Na, and K values remained unchanged. Subsequent administration of TZKD caused right atrial pressure and PaCO2 to increase and PaO2 to decrease, compared with values obtained after xylazine administration. Remaining cardiorespiratory, acid-base, hematologic, and electrolyte values did not differ from those obtained after xylazine administration. CONCLUSION: IV administration of TZKD induces short-term anesthesia in horses. Potential advantages of this drug combination are the small volume of drug administered; minimal cardiorespiratory depression; quality of induction and maintenance of, and recovery from, anesthesia; and duration of drug effects.     

Hemodynamic Effects of Atropine and Glycopyrrolate in Isoflurane-Xylazine-Anesthetlzed Dogs

Alterations in parasympathetic tone are partially responsible for xylazine's hemodynamic effects. The purpose of this study was to evaluate and compare the hemodynamic changes caused by the administration of intravenous (IV) atropine or glycopyrrolate after IV xylazine in isoflurane-anesthetized dogs. Six healthy beagles (8.2 to 10.7 kg) were used in two trials separated by 7 days. Anesthesia was induced and maintained with isoflurane in 100% oxygen with controlled ventilation. Once constant end-tidal isoflurane (1.8%) and arterial partial pressure of carbon dioxide (35 to 45 mm Hg) values were reached, baseline data were recorded and xylazine (0.5 mg/kg, IV) was given. In trial 1 atropine (0.1 mg/kg, IV) was given 5 minutes after xylazine, and in trial 2 glycopyrrolate (0.025, mg/kg, IV), was given 5 minutes after xylazine. Hemodynamic variables were recorded 3 minutes after xylazine and 3 minutes after anticholinergic administration. In trial 2, bilateral vagotomies were performed 10 minutes after glycopyrrolate, and hemodynamic variables were recorded 3 minutes later. Heart rate, cardiac index, and stroke index decreased; arterial pressure and systemic vascular resistance increased after xylazine. Heart rate, cardiac index, and rate pressure product increased after anticholinergic administration. Significant differences between atropine and glycopyrrolate were not observed in any of the hemodynamic parameters. Similarly, significant differences between glycopyrrolate and bilateral vagotomy were not observed. The authors conclude that intravenous atropine and glycopyrrolate have equivalent hemodynamic actions during the increased pressure phase after IV xylazine in isoflurane-anesthetized dogs; that intravenous atropine and glycopyrrolate produce comparable increases in heart rate and that both may increase the risk of myocardial hypoxia associated with an increase in rate pressure product; and that vagal blockade produced by high-dose glycopyrrolate (.025 mg/kg, IV) is similar to that produced by bilateral vagotomy.     

Effect of ether, ethanol and aqueous extracts of ginseng on cardiovascular function in dogs.

Ether, ethanol and aqueous extracts of ginseng were serially prepared from Korean ginseng plants. Each extract in the dose of 40 mg/kg was administered intravenously to ten dogs under light halothane anesthesia while 11 cardiovascular variables were compared during the ensuing two hours. The variable included cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit. Following the administration of the ether extract (40 mg/kg) the heart rate and the central venous pressure decreased significantly. The administration of ethanol extract (40 mg/kg) caused a significant decrease in the heart rate and the mean arterial pressure. After the administration of the aqueous extract (40 mg/kg) the cardiac output, stroke volume and central venous pressure were significantly decreased, while the total peripheral resistance was significantly increased.     

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.     

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 airway function in ponies with recurrent airway obstruction.

The effect of IV administration of the alpha 2-adrenoceptor agonist xylazine hydrochloride (0.5 mg/kg of body weight) was examined in ponies with recurrent obstructive pulmonary disease, commonly called heaves. Six ponies with the disease (principals) were studied during clinical remission and during an acute attack of airway obstruction precipitated by stabling and feeding of dusty hay. Six control ponies were also studied. In principal ponies with airway obstruction, xylazine administration significantly (P < 0.05) decreased pulmonary resistance and increased dynamic compliance, but did not affect PaO2 or PaCO2. The alpha 2-antagonist yohimbine blocked the pulmonary effects of xylazine. Administration of saline solution was without effect in both groups of ponies at all periods and xylazine did not have effect in controls or in principals in clinical remission.     

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.     

Caudal epidural analgesia induced by xylazine administration in cows

Xylazine (0.05 mg/kg of body weight diluted to a 5-ml volume, using 0.9% NaCl) or 5 ml of 0.9% NaCl was administered epidurally into the first caudal intervertebral space (Co1-Co2) in 8 cows (mean +/- SD body weight, 583 +/- 150 kg). Cows were observed for responses to deep needle pricking of the caudal dermatomes (S3 to Co), sedation, and ataxia. Heart rate, respiratory rate, body temperature, rate of ruminal contractions, coccygeal arterial blood pressure, pHa, blood gas tension (PaO2, PaCO2), base excess, total solids concentration, and PCV were determined before and after xylazine administration. Epidurally administered xylazine induced sedation and selective (S3 to Co) analgesia for at least 2 hours. Mild ataxia of hind limbs was observed in 6 cows, but all cows remained standing. Heart rate, respiratory rate, rate of ruminal contractions, arterial blood pressure, PaO2, PCV, and total solids concentration were significantly (P less than 0.05) decreased, and PaCO2, base excess, and bicarbonate concentration were significantly (P less than 0.05) increased after xylazine administration. Epidurally administered 0.9% NaCl did not alter sensory perception to needle pricking and did not affect any of the physiologic variables determined. Although epidural administration of xylazine induced analgesia and sedation in healthy cows, it should be avoided for epidural analgesia in cattle with heart disease, lung disease, and/or gastrointestinal disease because of its potent cardiopulmonary and ruminal depressant effects.     

Cardiopulmonary and behavioral effects of fentanyl-droperidol in cats

The combination of the narcotic fentanyl (0.4 mg/ml) and the tranquilizer droperidol (20 mg/ml) was injected into 12 healthy adult cats at a rate of 1 ml/9 kg of body weight, sc. Arterial blood pressure, heart rate, respiratory frequency, PaCO2, and PaO2, arterial pH (pHa), and rectal temperature were measured before and 30, 60, 90, and 120 minutes after injection of fentanyl-droperidol. Respiratory frequency was decreased significantly (P less than 0.05) and heart rate increased significantly (P less than 0.05) at all measurement intervals after drug administration. Observed decrements in arterial blood pressure were not significant. Arterial PO2, PCO2, and pH did not change significantly. A significant (P less than 0.05) decrease in body temperature was measured 90 minutes after drug administration. All cats were calm, tractable, and frequently assumed lateral recumbency after administration of fentanyl-droperidol. This maximal tranquil state was determined to be 30 to 60 minutes after drug administration.     

Cardiopulmonary effects of intramuscular xylazine-ketamine in calves.

The cardiopulmonary effects of an intramuscular xylazine (0.088 mg/kg)-ketamine (4.4 mg/kg) drug combination were evaluated in calves. Heart rate, central venous and mean pulmonary artery blood pressures, and cardiac output did not change after drug administration. Mean arterial blood pressure decreased significantly (P less than 0.05) 15 minutes after drug administration. Respiratory frequency increased significantly (P less than 0.05) whereas arterial partial pressure of oxygen (PaO2) decreased significantly (P less than 0.05) after drug administration. The duration of lateral recumbency was 55.7 +/- 10.4 minutes. Immediate or long-term adverse effects were not observed.     

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.     

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.     

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.     

A case of spontaneous venous embolism with carbon dioxide during laparoscopic surgery in a pig

BACKGROUND: Carbon dioxide (CO2) embolism is a possible complication of capnoperitoneum during laparoscopic surgery. Experimentally induced venous CO2 embolism has been studied in pigs. In this paper we report a case of spontaneous CO2 embolism. OBSERVATIONS: A 4-month-old Large White pig weighing 20 kg underwent experimental laparoscopic surgery under general anaesthesia. Monitoring consisted of pulse oximetry, capnography, airway pressure, electrocardiography, invasive arterial and central venous blood pressures, and arterial blood-gas analysis. Shortly after the start of laparoscopy and onset of CO2 insufflation, sudden decreases in end-tidal CO2 (Pe'CO2), haemoglobin saturation of oxygen (SpO2), systolic arterial blood pressure and heart rate were observed. Airway pressure increased and pulmonary compliance decreased simultaneously. Insufflation was immediately discontinued and epinephrine (2 mg IV), atropine (0.5 mg IV) and a 50 mL bolus of a polygeline solution were administered without effect. At this time arterial blood-gas analysis revealed a pH of 7.29 and a PaCO2 of 6.8 kPa (51.2 mmHg); PaO2 was 26.6 kPa (199.5 mmHg). After 4 minutes asystole occurred. CONCLUSIONS: The sudden decrease of Pe'CO2 and lung compliance combined with the sudden decrease in systolic blood pressure, heart rate and a poor response to resuscitation suggest a case of fatal gaseous venous embolism.     

CHANGES IN THE ACID BASE STATUS OF SHEEP ANAESTHETISED WITH A COMBINATION OF ATROPINE SULPHATE ACEPROMAZINE AND KETAMINE HYDROCHLORIDE

pH, PaCO2, PaO2, standard bicarbonate, base excess and reduced pH were measured in sheep before and at regular intervals after administration of ketamine with and without atropine and acepromazine premedication. A decrease in pH and PaO2 and a rise in PaCO2 was observed 15 minutes after administration of ketamine. Administration of atropine with and without acepromazine had no significant effect on pH, PaCO2 and PaO2. The values for standard bicarbonate, base excess and reduced pH were not significantly affected. This indicates that minor changes observed in pH, PaCO2 after ketamine administration are compensated for by the healthy animal's blood buffer system.     

Preliminary Results of Behavioral and Cardiopulmonary Effects of a Constant Rate Infusion of Remifentanil–Xylazine for Sedation in Horses

Standing surgical procedures are performed commonly in horses under sedation. The use of a xylazine and remifentanil combination has not been investigated in horses. We proposed to evaluate behavioral and cardiopulmonary effects of an intravenous (IV) infusion of xylazine with remifentanil for sedation in horses. Xylazine (0.8 mg/kg IV) followed in 3 minutes by remifentanil (0.0005 mg/kg IV), and a constant rate infusion of xylazine and remifentanil (0.65 mg/kg/h; 0.0225 mg/kg/h, respectively) was administered in three horses. Heart rate, respiratory rate (RR), arterial blood pressures, quality of sedation, pH, partial pressure of arterial CO₂ (PaCO₂), partial pressure of arterial O₂ (PaO₂), ataxia, sedation, and sedation overall outcome were assessed. Heart rate and RR remained within normal values during sedation without significant changes from baseline. Systolic, mean, and diastolic arterial blood pressures were increased during sedation. There were no significant changes in pH, PaCO₂, and PaO₂. Sedation developed immediately after injection of xylazine in the three horses but did not increase after remifentanil bolus or IV infusion of both drugs. None of the mares had ataxia. Adverse effects during and after sedation were present: excitement, increase in locomotor activity, and decrease in the gastrointestinal motility. The combination of xylazine and remifentanil sedation protocol produces adverse effects. This protocol cannot be recommended for clinical conditions, at the described doses.