Abstract

Six captive polar bears (Ursus maritimus) were immobilized to compare the effects of Telazol^® with a medetomidine-Telazol^® combination (MZT). Telazol^® was administered at an estimated dose of 6.5 mg/kg. Medetomidine was administered at an estimated dose of 52 µg/kg combined with tiletamine at an estimated dose of 0.86 mg/kg, and zolazepam at an estimated dose of 0.86 mg/kg. Animals immobilized with MZT appeared to be in a “deeper” plane of anesthesia than those anesthetized with Telazol^® alone. Heart rate, respiratory rate, PaO₂, and BE were significantly lower with MZT than with Telazol^® alone. Hypoxemia was present with MZT and was most severe at the 15-minute reading. Systolic, mean, and diastolic arterial pressure were significantly higher with MZT. Both combinations can be used to produce safe, effective immobilization, for at least 1 hour in polar bears.

Introduction

Telazol^® (zolazepam + tiletamine) is the drug of choice for immobilization of polar bears (Ursus maritimus). Reasons for the popularity of this drug combination include relatively small drug volume, rapid induction, and safe reliable immobilization.^6,9 The major disadvantage of Telazol^® is lack of reversibility and prolonged recovery. Medetomidine is a potent alpha-2 adrenoceptor agonist that has been used in combination with ketamine, to produce immobilization in a variety of domestic and non-domestic animals.^3-5,7,8,10 The sedative effects of medetomidine are readily reversed with atipamezole, a potent alpha-2 adrenoceptor antagonist. A “reversible” combination, such as this, is desirable in some situatuions.¹¹ Sudden recoveries from medetomidine-ketamine immobilization have been reported in brown bears.⁸ Following similar incidents of sudden recovery in polar bears immobilized with medetomidine-ketamine we developed a medetomidine-Telazol^® combination (MZT), in an attempt to decrease the risk of sudden recoveries.¹ A pilot study of the combination in black bears was performed.² The major side effects were hypertension and hypoxemeia.² The following study details the cardiopulmonary effects of (MZT) and Telazol^® in captive polar bears.

Materials and Methods

The bears immobilized in this study were six captive polar bears that were captured in Churchill, Canada, during October 1996, as part of the Manitoba Department of Natural Resources’ polar bear control program. These animals were captured at least 7 days prior to our experiments and were maintained individually in cages with access to fresh water only. Polar bears naturally fast at this time of the year, and in this area, had been without food since the ice melted in Hudson Bay, during early July.

Six bears were immobilized with both combinations. Initial choice of immobilizing combination was random. Treatments were administered at least 5 days apart. Immobilizing drugs were administered, with a pole syringe into the muscles of the shoulder or neck. Weight was estimated initially and following immobilization the bears were weighed to determine actual dose received. Medetomidine was administered at an estimated dose of 52 µg/kg. This was combined with tiletamine at an estimated dose of 0.86 mg/kg and zolazepam at an estimated dose of 0.86 mg/kg. These dosages were based on a pilot study in black bears² and on field studies of the combination¹. The medetomidine was reversed with atipamezole, which was administered at four times the medetomidine dose. Half of the atipamezole was administered IV and half was administered IM Telazol^® was administered at an estimated dose of 6.5 mg/kg. This dose was based on doses reported in the literature,^6,9 and on a field study of this combination.

Once the bear was immobilized it was removed from the cage and a 20-g, 5-cm catheter was placed in the femoral artery. The catheter was connected to a Baxter^® transducer, which was, in turn, connected to a Propaq 400^® monitor. The arterial line was used to measure heart rate, direct arterial pressure, and to remove arterial blood samples for blood gas analysis. A 14-g 6-cm catheter was placed in the jugular vein, and blood was removed for CBC and hemoglobin determination. A lead II ECG was constantly monitored to characterize arrhythmias. A Nellcor Durasensor DS-100A^® oximeter probe was placed on the tongue for constant monitoring of hemoglobin saturation. Respiratory rate was determined by observation of chest excursions. Rectal temperature was determined with a digital thermometer. One hour following administration of the immobilizing drugs the monitors were disconnected and the bear was returned to its cage. Immobilization produced by MZT was reversed with atipamezole, and bears receiving Telazol^® were maintained in sternal recumbency and recovered spontaneously. Repeated measures ANOVA was used to compare between treatments. One way ANOVA was used to compare differences over time within treatment groups. Comparison among means at specific time points was performed with a Bonferroni test. A significance level of p<0.05 was used in the analysis of the results.

Results

Calculation of the actual drug doses received by these bears (all reported values are mean ± SD) revealed that they received a dose of 74.8±11.8 µg/kg of medetomidine plus 2.2±0.3 mg/kg of Telazol^®. Reversal was achieved with a 261±105 µg/kg of atipamezole. The time from drug administration to immobilization was 3.7±2.7 minutes following administration of MZT. The actual dose of Telazol^® administered was 8.2±2 mg/kg. The time from drug administration to immobilization was 3.7±1 minutes. Animals immobilized with MZT appeared to be in a “deeper” plane of anesthesia than those anesthetized with Telazol^® alone. A pronounced spike in blood pressure and heart rate could be elicited when the nail be was compressed with a hemostat during immobilization with Telazol^®. No change in heart rate or blood pressure occurred with the same procedure during immobilization with MZT. No arrhythmias were noted with either of the treatments. Heart rate, respiratory rate, PaO₂, and BE were significantly lower with MZT. Systolic, mean, and diastolic arterial pressure were significantly higher with MZT. Physiologic data are listed in Tables 1 and 2.

Table 1. Physiologic data following the administration of medetomidine + tiletamine + zolazepam (mean ± SD)

^WSignificant difference within treatment (difference between 15- and 60-minute measurements)
^BSignificant difference between treatments

Table 2. Physiologic data following the administration of Telazol (mean ± SD)

^WSignificant difference within treatment (difference between 15- and 60-minute measurements)
^BSignificant difference between treatments

Discussion

Hypertension and bradycardia are common findings in animals anesthetized with medetomidine-based protocols. Hypertension results from peripheral activation of alpha-2 receptors. Bradycardia is likely due to reflex increase in vagal tone. Bradycardia can result in decreased cardiac output and oxygen delivery.^4,10 Similar cardiovascular changes were noted during medetomidine-ketamine immobilization of polar bears.³ PaO₂ was significantly lower with MZT. Animals were hypoxemic (PaO₂<60 mm Hg) at the 15-minute sampling time. PaO₂ was increased to above 60 mm Hg by the 30-minute blood gas sample. PaO₂ continued to increase over time with MZT. Oxygenation was similar in black bears immobilized with this combination.² Hypoxemia is common in ruminants immobilized with medetomidine-ketamine.^4,5,7 Ventilation perfusion mismatch with increased venous admixture is the most likely cause of hypoxemia.³ Respiratory depression was minimal. Normal PaCO₂ for most species ranges between 35–45 mm Hg. The highest PaCO₂ with Telazol^® was 48±3 mm Hg at the 15-minute reading. The highest PaCO₂ encountered with MZT was 47±4 mm Hg at the 30-minute reading. Application of a hemostat to the nail bed resulted in a significant spike in heart rate and blood pressure during immobilization with Telazol^®. Heart rate and blood pressure did not change significantly during application of the hemostat in animals immobilized with medetomidine-ketamine. This is a very crude test of analgesia, but it does suggest that analgesia is better with MZT.

Conclusion

Both of these combinations can be used to produce safe, effective immobilization, for at least 1 hour in polar bears. Hypoxemia was present with MZT and was most severe at the 15-minute reading. These animals were ventilating adequately (PaCO₂ 44±9 mm Hg at 15 minutes) and hypoxemia should respond to supplemental oxygen administration. Oxygenation was excellent with Telazol^®, it would still be good clinical practice to monitor saturation with a pulse oximeter and administer supplemental oxygen if hypoxemia is encountered.

Acknowledgments

The authors would like to thank C. Elliot, M. Ramsay, M. Swain, the Manitoba Department of Natural Resources, the Churchill Northern Studies Center, and the Churchill Health Center for their assistance with this study. The authors also thank Farmos Pharmaceuticals and Pfizer Animal Health for providing the medetomidine and atipamezole used in this study. M. Cattet gratefully acknowledges the financial support of the Medical Research Council of Canada and the United States National Science Foundation.

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