Effects of xylazine butorphanol on cecal arterial blood flow, cecal mechanical activity, and systemic hemodynamics in horses

A chronic model with an ultrasonic transit time blood flow probe and strain gauge force transducers implanted on the cecum was used to evaluate cecal mechanical activity and cecal arterial blood flow in 4 conscious adult horses. Intravenous administration of xylazine (1.1 mg/kg of body weight) significantly decreased heart rate and cardiac output, but significantly increased diastolic pulmonary arterial pressure, mean pulmonary arterial pressure, carotid arterial pressure, and central venous pressure. Lateral cecal arterial blood flow after xylazine administration was decreased substantially more than was cardiac output, suggesting that xylazine caused constriction of the cecal vasculature. This effect of xylazine may have resulted from either a direct effect of xylazine on the cecal vasculature or from reflex vasoconstriction attributable to reduced cardiac output. Intravenous administration of butorphanol tartrate (0.1 mg/kg) did not significantly alter the hemodynamic responses to xylazine. Cecal mechanical activity, as measured by the motility index, was decreased for 120 minutes after administration of xylazine and for 150 minutes after administration of xylazine/butorphanol.     

Doxapram: cardiopulmonary effects in the horse

The cardiopulmonary effects of 3 dosages of doxapram hydrochloride (0.275 mg/kg, 0.55 mg/kg, and 1.1 mg/kg, IV) were studied in 6 adult horses. Doxapram given IV significantly (P less than 0.05) decreased PaCO2 and increased respiratory rate, cardiac output arterial blood pressures (systolic, mean, and diastolic) arterial pH, and PaO2 at 1 minute after each dose was administered. Heart rate and mean and diastolic pulmonary arterial blood pressure were significantly (P less than 0.05) increased 1 minute after the 2 larger dosages of doxapram were given (0.55 mg/kg and 1.1 mg/kg, IV), but not after the smallest dosage was given. All measurements, except heart rate and cardiac output, had returned to base line by 5 minutes after each dosing. Heart rate remained significantly (P less than 0.05) increased 10 minutes after the 0.55 mg/kg dosage was given and 30 minutes after the 1.1 mg/kg dosage. Cardiac output remained significantly (P less than 0.05) increased at 10 minutes, 5 minutes, and 30 minutes after the 0.275, 0.55, and 1.1 mg/kg dosages, respectively, were given.     

Effects of dopamine administration on cecal mechanical activity and cecal blood flow in conscious healthy horses

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity of the circular and longitudinal muscle layers of the cecal body were measured in 7 conscious healthy horses during IV infusion of physiologic saline solution for 60 minutes (control), during a 60-minute IV infusion of dopamine (at dosages of 1, 2.5, and 5 micrograms/kg/min), and for 60 minutes after IV infusion of dopamine. The mean values for lateral cecal arterial blood flow during IV infusion of dopamine at a dosage of either 1 or 2.5 micrograms/kg/min were not significantly different from the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. The mean values for lateral cecal arterial blood flow, however, were significantly greater during IV infusion of dopamine at a dosage of 5 micrograms/kg/min than the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. Intravenous infusion of dopamine at 1 and 2.5 micrograms/kg/min did not significantly change the mean values for carotid arterial pressure. In contrast, the mean values for carotid arterial pressure were significantly less during IV infusion of dopamine at dosages of 2.5 and 5 micrograms/kg/min than during infusion of saline solution. The mean values for heart rate were not significantly altered by infusion of dopamine at a dosage of either 1 or 2.5 micrograms/kg/min, but infusion of dopamine at a dosage of 5 micrograms/kg/min significantly increased heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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

Xylazine and tiletamine-zolazepam anesthesia in horses

The cardiopulmonary and anesthetic effects of xylazine in combination with a 1:1 mixture of tiletamine and zolazepam were determined in 6 horses. Each horse was given xylazine IV or IM, as well as tiletamine-zolazepam IV on 4 randomized occasions. Anesthetics were administered at the rate of 1.1 mg of xylazine/kg of body weight, IV, 1.1 mg of tiletamine-zolazepam/kg, IV (treatment 1); 1.1 mg of xylazine/kg, IV, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 2); 1.1 mg of xylazine/kg, IV, 2.2 mg of tiletamine-zolazepam/kg, IV (treatment 3); and 2.2 mg of xylazine/kg, IM, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 4). Tiletamine-zolazepam doses were the sum of tiletamine plus zolazepam. Xylazine, when given IV, was given 5 minutes before tiletamine-zolazepam. Xylazine, when given IM, was given 10 minutes before tiletamine-zolazepam. Tiletamine-zolazepam induced recumbency in all horses. Duration of recumbency in group 1 was 31.9 +/- 7.2 (mean +/- 1 SD) minutes. Increasing the dosage of tiletamine-zolazepam (treatments 2 and 3) significantly (P less than 0.05) increased the duration of recumbency. Xylazine caused significant (P less than 0.05) decreases in heart rate and cardiac output and significant (P less than 0.05) increases in central venous pressure and mean pulmonary artery pressure 5 minutes after administration. Respiratory rate was decreased. Arterial blood pressures increased significantly (P less than 0.05) after xylazine was administered IV in treatments 1 and 3, but the increases were not significant in treatment 2. Xylazine administered IM caused significant (P less than 0.05) increases in central venous pressure and significant (P less than 0.05) decreases in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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

Analgesic and systemic effects of ketamine,xylazine, and lidocaine after subarachnoid administration in goats

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.     

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.     

Cardiac performance in cats after administration of xylazine or xylazine and glycopyrrolate: echocardiographic evaluations

Cardiac performance was evaluated in 9 healthy cats sedated with xylazine. Each cat was evaluated echocardiographically before and after the administration of xylazine or xylazine and glycopyrrolate. Each cat was echocardiographically evaluated during manual restraint only (control value), after IM administration of 0.55 mg of xylazine/kg of body weight, after IM administration of 2.2 mg of xylazine/kg, and after IM administration of 0.011 mg of glycopyrrolate/kg followed 10 minutes later by IM administration of 2.2 mg of xylazine/kg. Echocardiographic indices of cardiac performance (fractional shortening, left ventricular wall amplitude, aortic amplitude, mitral valve E point septal separation) indicated a significant decrease (P less than 0.05) in the left ventricular function and heart rate after the small (0.55 mg/kg) and large (2.2 mg/kg) dosages of xylazine. With the administration of glycopyrrolate, the bradycardia was minimized, but cardiac performance was not improved. After administration of glycopyrrolate, cardiac performance decreased, but the decrease was not significant when compared with the ventricular performance of the cats after administration of the large dosage of xylazine. Compared with control values, the reduction in left ventricular function values associated with administration of xylazine or xylazine and glycopyrrolate was independent of the heart rate. Therefore, the alpha-2 adrenergic agonist xylazine has a marked depressive effect on cardiac performance in the cat, and premedication with glycopyrrolate may not completely alleviate the undesirable bradycardia, but may actually be detrimental to the cardiovascular system.     

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

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

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.     

Evaluation of Three Midazolam-Xylazine Mixtures Preliminary Trials in Dogs

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

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

Xylazine and remifentanil in constant rate infusion (CRI) could be used for sedation in horses without adverse effects. The objective was to evaluate behavioral and cardiopulmonary effects of an intravenous (IV) infusion of xylazine and remifentanil for sedation in horses. Xylazine (0.8 mg/kg IV) followed after 3 minutes by a CRI of xylazine and remifentanil (0.65 mg/kg/h and 6 μg/kg/h, respectively) was administered in 10 healthy horses for 60 minutes. Sedation, ataxia, and cardiopulmonary, hematological, and blood gases variables were evaluated. Heart rate decreased significantly during the first 25 minutes after CRI of xylazine and remifentanil, whereas the respiratory rate showed a significant decrease at 20 minutes and remained significantly low until the endpoint. There were no statistically significant fluctuations in blood arterial pressure, blood pH, partial pressure of arterial carbon dioxide, lactate, creatinine, calcium, chlorine, and sodium, compared with baseline values. Blood partial pressure of arterial oxygen and bicarbonate values were significantly higher compared with baseline values, whereas potassium decreased. Sedation and ataxia developed immediately after the administration of xylazine in all horses. All horses recovered successfully within 10 minutes after interruption of the CRI of xylazine and remifentanil, with no ataxia. No adverse effects were observed. The use of a combination of xylazine and remifentanil as sedation protocol has no adverse effects at the described dosage.     

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.     

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.     

Effect of yohimbine on xylazine-ketamine anesthesia in cats

Xylazine and ketamine are an anesthetic combination used in feline practice for routine surgical procedures. In a controlled study, we evaluated the effects of yohimbine, an antagonist of xylazine, on the anesthesia induced by this anesthetic combination in cats. Two intramuscular doses of xylazine and ketamine (2.2 mg of xylazine/kg plus 6.6 mg of ketamine/kg and 4.4 mg of xylazine/kg plus 6.6 mg of ketamine/kg) caused approximately 60 and 100 minutes of anesthesia, respectively, in control cats. When yohimbine (0.1 mg/kg) was given intravenously 45 minutes after ketamine administration, the cats regained consciousness within 3 minutes. They were ambulatory 1 to 2 minutes after regaining consciousness. Yohimbine also reversed the bradycardia and respiratory depression elicited by xylazine-ketamine. The results indicated that yohimbine may be useful for controlling the duration of xylazine-ketamine anesthesia in cats.     

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.     

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.     

Clinical and pathological effects of flunixin meglumine administration to neonatal foals.

The effects of daily intravenous administration of flunixin meglumine at dosages of 0.55, 1.1, 2.2 and 6.6 mg/kg for five days were examined in neonatal foals. Six two day old foals were used to evaluate the effect of each dosage. Foals were examined every day and blood samples collected on days 1, 3 and 6. All foals were euthanized after six days, necropsied and examined for lesions. The major clinical abnormality was diarrhea, but the incidence was not related to the dosage of flunixin meglumine administered. The foals receiving 6.6 mg/kg of flunixin meglumine had significantly more gastrointestinal ulceration and greater cecal pathology and cecal petechiation scores than those foals treated with saline. The foals in the 6.6 mg/kg treatment group had a greater loss of total protein during the study, but the difference was not significant. There were no statistically significant blood cellular or biochemical alterations associated with the administration of flunixin meglumine. There were no significant clinicopathological differences between healthy foals treated with the recommended dosage of flunixin meglumine and those treated with physiological saline.     

Evaluation of Nociception,Sedation, and Cardiorespiratory Effects of a Constant Rate Infusion of Xylazine Alone or in Combination with Lidocaine in Horses

This study aimed to evaluate the effects of a constant rate infusion (CRI) of xylazine or xylazine in combination with lidocaine on nociception, sedation, and physiologic values in horses. Six horses were given intravenous (IV) administration of a loading dose (LD) of 0.55 mg/kg of xylazine followed by a CRI of 1.1 mg/kg/hr. The horses were randomly assigned to receive three treatments, on different occasions, administered 10 minutes after initiation of the xylazine CRI, as follows: control, physiologic saline; lidocaine low CRI (LLCRI), lidocaine (LD: 1.3 mg/kg, CRI: 0.025 mg/kg/min); and lidocaine high CRI (LHCRI), lidocaine (LD: 1.3 mg/kg, CRI: 0.05 mg/kg/min). A blinded observer assessed objective and subjective data for 50 minutes during the CRIs. In all treatments, heart and respiratory rates decreased, end-tidal carbon dioxide concentration increased, and moderate to intense sedation was observed, but no significant treatment effect was detected in these variables. Ataxia was significantly higher in LHCRI than in the control treatment at 20 minutes of infusion. Compared with baseline values, nociceptive threshold increased to as much as 79% in the control, 190% in LLCRI, and 158% in LHCRI. Nociceptive threshold was significantly higher in LLCRI (at 10 and 50 minutes) and in LHCRI (at 30 minutes) than in the control treatment. The combination of CRIs of lidocaine with xylazine produced greater increases in nociceptive threshold compared with xylazine alone. The effects of xylazine on sedation and cardiorespiratory variables were not enhanced by the coadministration of lidocaine. The potential to increase ataxia may contraindicate the clinical use of LHCRI, in combination with xylazine, in standing horses.