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Evaluation of the sedative and cardiorespiratory effects of medetomidine, medetomidine-butorphanol, medetomidine-ketamine, and medetomidine-butorphanol-ketamine in ferrets.

Ten ferrets were used in a crossover study to determine the anesthetic effects of intramuscular (I.M.) medetomidine (80 microg/kg body weight), medetomidine (80 microg/kg body weight)-butorphanol (0.1 mg/kg body weight), medetomidine (80 microg/kg body weight)-ketamine (5 mg/kg body weight), and medetomidine (80 microg/kg body weight)-butorphanol (0.1 mg/kg body weight)-ketamine (5 mg/kg body weight). All ferrets assumed lateral recumbency within four minutes and remained dorsally recumbent for 100 minutes, until atipamezole (400 microg/kg body weight, I.M.) administration. All four anesthetic combinations were effective for chemical restraint, with the most respiratory depression occurring in the medetomidine-butorphanol-ketamine group. The addition of butorphanol or ketamine to medetomidine significantly increased the duration of analgesia. The addition of ketamine to medetomidine-butorphanol expedited endotracheal intubation.

Analgesics, Opioid↗

Sedative and cardiorespiratory effects of medetomidine, medetomidine-butorphanol, and medetomidine-ketamine in dogs.

OBJECTIVE: To determine sedative and cardiorespiratory effects of i.m. administration of medetomidine alone and in combination with butorphanol or ketamine in dogs. DESIGN: Randomized, crossover study. ANIMALS: 6 healthy adult dogs. PROCEDURES: Dogs were given medetomidine alone (30 micrograms/kg [13.6 micrograms/lb] of body weight, i.m.), a combination of medetomidine (30 micrograms/kg, i.m.) and butorphanol (0.2 mg/kg [0.09 mg/lb], i.m.), or a combination of medetomidine (30 micrograms/kg, i.m.) and ketamine (3 mg/kg [1.36 mg/lb], i.m.). Treatments were administered in random order with a minimum of 1 week between treatments. Glycopyrrolate was given at the same time. Atipamezole (150 micrograms/kg [68 micrograms/lb], i.m.) was given 40 minutes after administration of medetomidine. RESULTS: All but 1 dog (given medetomidine alone) assumed lateral recumbency within 6 minutes after drug administration. Endotracheal intubation was significantly more difficult when dogs were given medetomidine alone than when given medetomidine and butorphanol. At all evaluation times, percentages of dogs with positive responses to tail clamping or to needle pricks in the cervical region, shoulder region, abdominal region, or hindquarters were not significantly different among drug treatments. The Paco2 was significantly higher and the arterial pH and Pao2 were significantly lower when dogs were given medetomidine and butorphanol or medetomidine and ketamine than when they were given medetomidine alone. Recovery quality following atipamezole administration was unsatisfactory in 1 dog when given medetomidine and ketamine. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that a combination of medetomidine with butorphanol or ketamine resulted in more reliable and uniform sedation in dogs than did medetomidine alone.

Adjuvants, Anesthesia↗

Comparison of sedative effects induced by medetomidine, medetomidine-midazolam and medetomidine-butorphanol in dogs.

Sedative effects of combinations of medetomidine at 20 micrograms/kg--midazolam at 0.3 mg/kg (Me-Mi) and medetomidine at 20 micrograms/kg--butorphanol at 0.1 mg/kg (Me-B) were evaluated comparing with those of medetomidine alone (20, 40 and 80 mu/kg). All dogs given Me-Mi or Me-B were smoothly and rapidly induced to more profound and longer sedation than those by medetomidine alone. Especially, Me-Mi produced desirable sedation with moderate reflex depression, analgesia, excellent muscle relaxation and immobilization without further side effects. This potent effect of this combination seemed to be induced by a synergistic interaction between medetomidine and midazolam. This combination is available and valuable as a chemical restraint agent in dogs for various diagnostic or therapeutic procedures accompanied by light pain.

Animals↗

Cardiopulmonary effects of medetomidine, medetomidine-midazolam and medetomidine-midazolam-atipamezole in dogs.

Cardiopulmonary effects of medetomidine (20 micrograms/kg)-midazolam (0.3 mg) (Me-Mi) were compared with those of medetomidine alone (80 micrograms/kg) (Me80) in dogs. The intramuscular administration of this combination caused bradycardia and transient mild pressor response. Heart rate decreased soon after the administration and remained significantly below the baseline value with average values of 50-70 beats/min. Blood pressure increased to its maximum within 5 to 10 min then decreased gradually. Cardiac index decreased corresponding the decrease in heart rate. However these changes were less profound than those of Me80 indicating significantly higher values in cardiac index and lower values in systemic vascular resistance. Effects on the respiratory function were slight. The reduction of the dose of medetomidine to one-fourth in Me-Mi was effective to reduce the adverse effect of medetomidine, especially in peripheral vasoconstriction. Atipamezole effectively reversed cardiopulmonary effects induced by medetomidine-midazolam. Heart rate and cardiac index increased and systemic vascular resistance decreased significantly after administration of atipamezole. The possible use of an antagonist as a reversal agent might enhance the value and availability of medtomidine-midazolam as a chemical restraint agent in dogs.

Adrenergic alpha-Antagonists↗

Quantitative electroencephalography of medetomidine, medetomidine-midazolam and medetomidine-midazolam-butorphanol in dogs.

The purpose of this study was to evaluate the effects of the administration of an alpha2-adrenoceptor agonist alone and in combination with other derivatives on brain wave activity. In addition, the diagnostic values of the electroencephalogram (EEG) for judging the depth of the balanced anaesthesia with an alpha2-adrenoceptor agonist was evaluated. The treatments comprised 20 microg/kg medetomidine (Me-20), 80 microg/kg medetomidine (Me-80), 20 microg/kg medetomidine and 0.5 mg/kg midazolam (Me-Mi) administered intramuscularly, and 20 microg/kg medetomidine with 0.5 mg/kg midazolam and 0.1 mg/kg butorphanol (Me-Mi-Bu). The EEG was recorded continuously at pre-administration, and at 7, 10, 20, 30, 45 and 60 min after administration. The recorded data were analysed by separating the power spectrum into 1-3, 4-7, 8-13 and 14-30 Hz bands. Spectral-edge analysis was used to calculate the spectral edge frequency 90 (SEF90) and the median edge frequency (MEF). Time-related changes in power spectrum analysis showed a significant increase in the Me-80 group in the 1-3 Hz band. The power for 1-3 Hz in the Me-80 group was significantly higher than in all the other groups. In the 14-30 Hz band, there was a significant reduction of power in all groups following administration of the agents. The SEF90 frequencies were significantly reduced in all groups except for the Me-20 group after administration of the agents. The SEF90 frequencies in the Me-20, Me-Mi and Me-Mi-Bu were all significantly higher than those in the Me-80 group. However, there was no significant difference between the Me-20, Me-Mi and Me-Mi-Bu groups in any analyses. Our results demonstrated that the changes in quantitative EEG made by the Me-Mi-Bu and Me-Mi groups were similar to those made by Me-20 groups. Present results suggest that the EEG should be interpreted with caution in assessing the anaesthetic level in balanced anaesthesia in dogs.

Adrenergic alpha-Agonists↗

Cardiorespiratory effects of medetomidine-butorphanol, medetomidine-butorphanol-diazepam, and medetomidine-butorphanol-ketamine in captive red wolves (Canis rufus).

Safe, effective, and reversible immobilization protocols are essential for the management of free-ranging red wolves (Canis rufus). Combinations using an alpha2-adrenoceptor agonist and ketamine have been shown to be effective for immobilization but are not reversible and can produce severe hypertension and prolonged or rough recoveries. To minimize hypertension and provide reversibility, 24 red wolves were immobilized using three medetomidine-butorphanol (MB) combinations without the use of ketamine in the initial injection. All wolves were administered medetomidine (0.04 mg/kg i.m.) and butorphanol (0.4 mg/kg i.m.). Seven wolves received no other immobilization agents (MB wolves), nine received diazepam (0.2 mg/kg i.v.) at the time they were instrumented (MBD wolves), and eight received ketamine (1 mg/kg i.v.) 30 min after instrumentation (MBK30 wolves). Physiologic parameters were monitored during immobilization. The heart rate was similar among the three groups for the first 30 min, and marked bradycardia was noted in one wolf from each group. Hypertension was observed initially in all three groups but was resolved within 10-30 min. The MBK30 wolves had significant elevations in heart rate and transient hypertension after intravenous ketamine administration. Most wolves had mild to moderate metabolic acidemia. Immobilizing drugs were antagonized in all wolves with atipamezole (0.2 mg/kg i.m.) and naloxone (0.02 mg/kg i.m.). The medetomidine-butorphanol-diazepam wolves were also given flumazenil (0.04 mg/kg i.v.). All wolves were standing within 12 min and were fully recovered within 17 min. Medetomamine-butorphanol and MBD combinations provided effective and reversible immobilization of red wolves without the sustained hypertension associated with the use of alpha2-adrenoceptor agonist-ketamine combinations. Delaying the administration of ketamine reduced its hypertensive effects.

Adrenergic alpha-Antagonists↗

A comparison of medetomidine-propofol and medetomidine-midazolam-propofol anesthesia in rabbits.

We evaluated and compared the effects of medetomidine-propofol and medetomidine-midazolam-propofol anesthesia in rabbits. Fourteen New Zealand White rabbits were randomly assigned to receive either medetomidine (0.25 mg/kg, i.m.)-atropine (0.5 mg/kg, i.m.)-propofol (4 mg/kg, i.v.) (n = 7) or medetomidine (0.25 mg/kg, i.m.)-atropine (0.5 mg/kg, i.m.)-midazolam (0.5 mg/kg, i.m.)-propofol (2 mg/kg, i.v.) (n = 7). Five minutes after medetomidine-atropine or medetomidine-atropine-midazolam i.m. injection, propofol was administered i.v. Both medetomidine and medetomidine-midazolam rapidly (within 5 minutes) immobilized all rabbits and greatly eased the i.v. administration of propofol. Endotracheal intubation was accomplished easily after propofol injection in both groups. There was no significant difference between medetomidine-propofol and medetomidine-midazolam-propofol-treated rabbits in heart rate, respiratory rate, mean arterial pressure, or end-tidal CO2. The addition of midazolam to the medetomidine-propofol regimen significantly (P < 0.05) prolonged the duration of ear-pinch analgesia (25.0 +/- 7.1 vs. 36.7 +/- 8.9 minutes), the time from extubation to sternal recumbency (0.0 vs. 26.7 +/- 8.1 minutes), and the time from extubation to standing (0.0 vs. 39.5 +/- 11.3 minutes) without inducing significant changes in arterial blood pressure and end-tidal alveolar CO2. We consider both medetomidine-propofol and medetomidine-midazolam-propofol combinations to be safe and effective regimens for induction and short-term anesthesia in rabbits.

Anesthesia, General↗

Comparison of sedative and cardiorespiratory effects of medetomidine and medetomidine-butorphanol combination in dogs.

OBJECTIVE: Sedative, cardiorespiratory, and analgesic effects of intramuscular administration of medetomidine (40 micrograms/kg of body weight)-glycopyrrolate (0.01 mg/kg) and medetomidine (10 micrograms/kg)-butorphanol (0.2 mg/kg)-glycopyrrolate (0.01 mg/kg) combinations were compared. Additional evaluations were done on reversal of medetomidine, using atipamezole (200 micrograms/kg. IV), after 90 minutes of medetomidine-induced sedation. DESIGN: Crossover study, with each dog receiving each drug combination at 1-week intervals. ANIMALS: Six 2-year-old English hound-type dogs. PROCEDURE: Arterial blood pressure, ECG, respiratory rate, tidal volume, minute volume, arterial blood gas tensions, and serum biochemical variables were measured before, during, and after sedation. Analgesia was evaluated by needle prick on the skin and tail clamp. RESULTS: Heart rate decreased significantly from 100 beats/min to < 40 beats/min within 3 minutes of injection of medetomidine and medetomidine and butorphanol (MB). Mean arterial blood pressure in both groups were maintained above 100 mm of Hg throughout the recording period. There was no significant difference between medetomidine and MB in respiratory rate, tidal volume, and minute ventilation. Hypoxemia (PaO2 < 60 mm of Hg) was observed at 10 and 20 minutes in 2 dogs given MB. Atipamezole administration in the dogs given medetomidine significantly increased PaO2, and returned the values to baseline. Needle prick analgesia duration was longer in the medetomidine (80 +/- 7.7 minutes) than MB (56.0 +/- 19.2 minutes) group. Tail pinch analgesia was variable in both groups. Duration of lateral recumbency was longer after medetomidine (90 +/- 0 minutes) than MB (73.5 +/- 19.0 minutes). CONCLUSION: Medetomidine and MB were effective combination for mildly invasive procedures. CLINICAL RELEVANCE: MB induced a shorter period of analgesia and recumbency than did medetomidine.

Analgesics, Opioid↗

Duration of nonresponse to noxious stimulation after intramuscular administration of butorphanol, medetomidine, or a butorphanol-medetomidine combination during isoflurane administration in dogs.

OBJECTIVE: To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO). ANIMALS: 6 healthy dogs. PROCEDURE: Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 microg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 microg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, end-tidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected. RESULTS: Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean +/- SD) was 0.0+/-0.0, 1.5+/-1.5, 2.63+/-0.49, and 5.58+/-2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone. CONCLUSION AND CLINICAL RELEVANCE: During ISO-induced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone.

Analgesics, Non-Narcotic↗

Effects of intramuscular administration of low doses of medetomidine and medetomidine-butorphanol in middle-aged and old dogs.

OBJECTIVE: To determine effects of low doses of medetomidine administered with and without butorphanol and glycopyrrolate to middle-aged and old dogs. DESIGN: Prospective randomized clinical trial. ANIMALS: 88 healthy dogs > or = 5 years old. PROCEDURE: Dogs were assigned randomly to receive medetomidine (2, 5, or 10 micrograms/kg [0.9, 2.3, or 4.6 micrograms/lb] of body weight, i.m.) alone or with glycopyrrolate (0.01 mg/kg [0.005 mg/lb], s.c.), medetomidine (10 micrograms/kg) and butorphanol (0.2 mg/kg [0.1 mg/lb], i.m.), or medetomidine (10 micrograms/kg), butorphanol (0.2 mg/kg), and glycopyrrolate (0.01 mg/kg). Anesthesia was induced with thiopental sodium and maintained with isoflurane. Degree of sedation and analgesia were determined before and after medetomidine administration. Respiratory rate, heart rate, and mean arterial blood pressure were determined 10 and 30 minutes after medetomidine administration. Adverse effects and amounts of thiopental and isoflurane used were recorded. RESULTS: Sedation increased after medetomidine administration in 79 of 88 dogs, but decreased in 7 dogs that received 2 or 5 micrograms of medetomidine/kg. Mean postsedation analgesia score and amounts of thiopental and isoflurane used were less in dogs that received medetomidine and butorphanol, compared with other groups. Respiratory rate, heart rate, and blood pressure were not different among groups. Significantly more adverse effects developed in dogs that did not receive glycopyrrolate. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of medetomidine (10 micrograms/kg, i.m.) and butorphanol (0.2 mg/kg, i.m.) induced sedation and analgesia and reduced amounts of thiopental and isoflurane required for anesthesia in middle-aged and old dogs. Glycopyrrolate decreased frequency of medetomidine-associated adverse effects.

Adjuvants, Anesthesia↗

A comparison between medetomidine-ketamine and medetomidine-propofol anaesthesia in rabbits.

We investigated the effects of combinations of the alpha 2-agonist medetomidine with either ketamine or propofol for their overall quality of anaesthesia, including the possible concomitant changes in respiratory and circulatory function in New Zealand White rabbits. Medetomidine was administered at 0.35 mg/kg, intramuscularly. Following sedation, ketamine (5 mg/kg) or propofol (2 and 3 mg/kg) were administered intravenously via the ear vein. Data on reflexes (palpebral, corneal, ear-pinch and toe-pinch), jaw muscle tone and physiologic parameters (heart rate, blood pressure, respiration rate, body temperature) were recorded before and after administration of drugs. Intermittent arterial blood sampling was performed at predetermined intervals before and after anaesthesia. The results show that the ear-pinch and toe-pinch reflexes and the jaw muscle tone are reliable indices to determine surgical anaesthetic depth. A surgical level of anaesthesia could be obtained reliably with the combination medetomidine-ketamine and medetomidine-propofol (3 mg/kg) with a duration of 19 min (variation 10 to 40 min, n = 6) and 11 min (variation 5 to 15 min, n = 6), respectively. Propofol administered at 2 mg/kg did not produce an adequate anaesthetic level. The data from this study demonstrate a high degree of predictability in achieving a fast induction and adequate anaesthetic depth together with a low incidence of untoward side-effects and a zero mortality with the combinations investigated. The data from the medetomidine-ketamine group show that, although adequate anaesthetic depth of medium duration is achieved, the arterial oxygen tension is reduced to hypoxemic levels. With the use of this combination, the supplemental administration of oxygen is advised. With the combination of medetomidine-propofol (3 mg/kg) a short duration anaesthesia of adequate depth was achieved, whereby physiological variables all remained within acceptable ranges. The use of medetomidine-propofol, in combination with the alpha 2-antagonist atipamezole to shorten recovery time, will provide reliable and very versatile anaesthesia in rabbits.

Anesthesia, General↗

Reversal of medetomidine-induced sedation in reindeer (Rangifer tarandus tarandus) with atipamezole increases the medetomidine concentration in plasma.

The pharmacokinetics of two potent alpha 2-adrenoceptor agents that can be used for immobilization (medetomidine) and reversal (atipamezole) of the sedation in mammals, were studied in three reindeer (Rangifer tarandus tarandus) in winter and again in summer. Medetomidine (60 micrograms/kg) was injected intravenously (i.v.), followed by atipamezole (300 micrograms/kg) intravenously 60 min later. Drug concentrations in plasma were measured by HPLC. The administration of atipamezole resulted in an immediate 2.5-3.5 fold increase in the medetomidine concentration in plasma. Clearance for medetomidine (median 19.3 mL/min.kg) was lower than clearance for atipamezole (median 31.0 mL/min.kg). The median elimination half-lives of medetomidine and atipamezole in plasma were 76.1 and 59.9 min, respectively. The animals became resedated 0.5-1 h after the reversal with atipamezole. Resedation may be explained by the longer elimination half-life of medetomidine compared to atipamezole.

Adrenergic alpha-Antagonists↗

Comparative physiologic effects of telazol, medetomidine-ketamine, and medetomidine-telazol in captive polar bears (Ursus maritimus).

The cardiopulmonary effects of three drug combinations in polar bears (Ursus maritimus) were studied. In 1995, five adult polar bears received i.m. injections of either 8.2 +/- 1.3 mg/kg of Telazol or a combination of 159 +/- 34 microg/kg of medetomidine with 4 +/- 0.8 mg/kg of ketamine in a crossover design. Significantly higher mean arterial pressure, lower heart rate, and lower partial pressure of arterial oxygen (Pao2) occurred with medetomidine-ketamine. In 1996, six adult polar bears were immobilized with i.m. injections of either 8.2 +/- 2 mg/kg of zolazepam-tiletamine or a combination of 74.8 +/- 11.8 microg/kg of medetomidine plus 2.2 +/- 0.3 mg/kg of zolazepam-tiletamine in a crossover design. Significantly higher mean arterial pressure and lower heart rate, base excess, and Pao2 occurred with medetomidine-zolazepam-tiletamine compared with zolazepam-tiletamine alone. Hypertension, bradycardia, and decreased Pao2 were observed with both medetomidine-ketamine and medetomidine-zolazepam-tiletamine. Both combinations should be well tolerated by healthy bears, but both have the potential to produce adverse effects in animals with cardiopulmonary disease. Zolazepam-tiletamine produced minimal adverse cardiopulmonary effects, consistent with the wide margin of safety of this combination in bears. The analgesic effect of zolazepam-tiletamine was apparently poor on the basis of the marked increases in pulse rate and mean arterial pressure after noxious stimuli.

Anesthetics, Combined↗

Medetomidine- and medetomidine-ketamine-induced immobilization in blue foxes (Alopex lagopus) and its reversal by atipamezole.

The sedative and immobilizing effects of the alpha 2-adrenoceptor agonist medetomidine alone or combined with the dissociative anesthetic ketamine, were studied in blue foxes. Medetomidine at doses of 25 and 50 micrograms/kg induced moderate to deep sedation, but only with the highest medetomidine dose tested, 100 micrograms/kg, was the immobilization complete. Medetomidine 50 micrograms/kg combined with ketamine 2.5 mg/kg rapidly induced complete immobilization, characterized by good myorelaxation, and no clinically significant alterations in serially determined hematologic and serum chemistry parameters. The alpha 2-adrenoceptor antagonist atipamezole effectively reversed the medetomidine- or medetomidine-ketamine-induced immobilizations. A transient increase in heart rates was noted after each atipamezole injection.

Adrenergic alpha-Antagonists↗

Immobilization of Norwegian reindeer (Rangifer tarandus tarandus) and Svalbard Reindeer (R. t. platyrhynchus) with medetomidine and medetomidine-ketamine and reversal of immobilization with atipamezole.

The sedative action of medetomidine (-ketamine) was studied in 12 captive Norwegian semidomesticated reindeer (NR), including 4 newborn calves, and in 7 free-living Svalbard reindeer (SR). Medetomidine, with or without ketamine, caused effective, reliable immobilization in NR. Doses of 50-200 micrograms/kg medetomidine alone or 30-125 micrograms/kg medetomidine combined with greater than or equal to 300 micrograms/kg ketamine induced complete immobilization, good muscle relaxation and persistent, deep sedation with little respiratory depression in NR; SR required higher doses. Atipamezole successfully antagonized medetomidine (-ketamine) resulting in rapid and persistent reversal of immobilization in all cases (NR and SR). Both medetomidine and atipamezole had wide safety margins and no conspicuous lasting side effects after reversal.

Adrenergic alpha-Antagonists↗

Pharmacokinetics of medetomidine in ponies and elaboration of a medetomidine infusion regime which provides a constant level of sedation.

The pharmacokinetics of intravenous (i.v.) medetomidine (7 mcg kg(-1)) were best described by a two-compartment model in five ponies. Total body clearance was 4 (SD 0.60) 1 kg h,(-1)t(1/2alpha)7. 6 (0.91) minutes and t(1/2beta)51.3 (13.09) minutes. In one pony the one-compartmental model was best fit, and total body clearance was 4. 2 l kg h(-1)and t(1/2)was 11 minutes. Medetomidine plasma levels had fallen below the limits of quantification (0.05 ng ml(-1)) within 4 hours. Medetomidine 5 mcg kg(-1)i.v. followed by an infusion of 3.5 mcg kg h(-1)for two hours provided a constant level of sedation reaching steady state plasma medetomidine levels of 1-1.5 ng ml(-1)within 30 minutes. Sedation was reversed effectively by atipamezole (60 mcg kg(-1)) i.v. The pharmacokinetics of medetomidine make it suitable for prolonged use by infusion, such as is required as part of a total intravenous anaesthetic technique in horses.

Animals↗

Cardiopulmonary effects of medetomidine-midazolam and medetomidine-midazolam- atipamezole in laboratory pigs.

The cardiopulmonary effects of medetomidine (40 micrograms/kg)-midazolam (0.2 mg/kg) and medetomidine (40 micrograms/kg)-midazolam (0.2 mg/kg)-atipamezole (160 micrograms/kg) were evaluated in laboratory pigs. The intramuscular administration of medetomidine-midazolam caused a pressor response, characterized by a rapid increase in arterial and pulmonary arterial pressure mediated mainly through systemic and pulmonary vasoconstriction. These pressures decreased after reaching a peak 5 to 10 min after the administration of sedatives, but maintained higher values than the base-line. However, all these changes caused by medetomidine-midazolam were within the physiological fluctuation. In addition, this combination did not induce bradycardia, subsequent hypotension or a significant decrease in cardiac output, which were generally observed with alpha 2-adrenoceptor agonists, and caused fewer changes in the respiratory system. The administration of atipamezole resulted in a marked transient decrease in vascular resistance, and caused a decrease in blood pressure and increases in cardiac output and heart rate. However, these changes were relatively small and sustained for a short time. Thus the combination of medetomidine-midazolam and atipamezole have minimal cardiopulmonary effects and might be used safely in laboratory pigs.

Adrenergic alpha-Agonists↗

The use of medetomidine, medetomidine-ketamine combinations and atipamezole at Helsinki Zoo--a review of 240 cases.

Medetomidine, medetomidine-ketamine combinations and/or atipamezole were used during 240 immobilizations of 32 non-domestic animal species. Medetomidine-ketamine induced reliable immobilization with good physiological quality in a variety of species. Atipamezole was effective in reversing the medetomidine, medetomidine-ketamine or xylazine induced immobilization.

Adrenergic alpha-Agonists↗