• Journal of Veterinary Clinics
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• v.20 no.3
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• pp.286-293
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• 2003

The cardiopulmonary and antagonistic effects of atipamezole, to medetomidine (30 ug/kg, IM)-tiletamine/zolazepam (10 mg/kg, IV) were determined. Twelve healthy mongrel dogs ,(4.00$\pm$0.53 kg, mean$\pm$SD) were randomly assigned to the four experimental groups (control, A30; atipamezole 30 ug/kg, A60; atipamezole 60 ug/kg, A150; atipamezole 150 ug/kg) with 3 dogs in each group. Atropine (0.03 mg/kg, IM), medetomidine, and tiletamine/zolazepam (TZ) were injected 10 minute intervals. Atipamezole was injected intravenously 15 minutes after TZ injection. Mean arousal time (MAT) was 52.50$\pm$4.98, 43.06$\pm$2.60, 32.83$\pm$8.13, and 14.36$\pm$1.60 minutes in control, A30, A60, and Al50 groups respectively. In Al50 group, MAT was significantly reduced (P < 0.05). but mean walking time (MWT) was similar to that in control group. In recovery period, the higher doses of atimapezole, the rougher recovery including head rocking, hypersalivation, and muscle twitching. Five of twelve dogs vomited within 5 minutes after medetomidine injection. In Control group, heart rate significantly decreased in all recording stages except 15 minutes after TZ injection, 10 minutes after medetomidine injection in all groups, and 40 minutes after atipamezole injection in A30 group (P < 0.05). In Al50 group, atipamezole reversed the respiratory depression induced by medetomidine. Arterial blood pressure was significantly decreased 10minutes after medetomidine injection and 15 minutes after TZ injection in almost dogs in this study (P < 0.05). From 10 minutes after atipamezole injection to arousal time, arterial blood pressure was progressively increased in A60 and A150 group. Any value of blood gas analysis and CBC, and serum chemistry values were not significantly changed except pH of Al50 at 10 minutes after medetomidine injection. As shown in present study, atipamezole(150 ug/kg) is considered to exert a useful reversal effect in dogs anesthetized with medetomidine-tiletamine/zolazepam combination.

• Journal of Veterinary Clinics
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• v.28 no.3
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• pp.291-296
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• 2011

The aims of the present study were to investigate the anesthetic and hemodynamic effects of medetomidine-ketamine combination and to compare antagonistic effects of atipamezole and yohimbine on the recovery of pig from anesthesia induced by medetomidine-ketamine combination. Landrace and Yorkshire cross-bred pigs were evaluated in the present study. Pigs (n = 8) received three different treatments (one treatment per 14 days in a random order). All pigs were injected intramuscularly with medetomidine, and ketamine in a single syringe. Intravenous injections of atipamezole (MKA), yohimbine (MKY), or a control saline solution (MK) were administered 20 minutes after the medetomidine-ketamine combination injection. The intravenous antagonist injections quickly reversed the medetomidine-ketamine induced sedation in the pigs, resulting in a significantly shorter duration of anesthesia in the MKA and MKY groups compared to the MK group. Mean arterial pressure (MAP) levels were significantly lower in the MKA and MKY groups compared to the MK group. Scores for posture and responses to noxious stimuli after atipamezole and yohimbine administration were significantly lower in the MKA and MKY groups than in the MK. In conclusion, the sedative effects and increases in blood pressure induced by a medetomidine-ketamine combination were quickly and smoothly reversed by atipamezole or yohimbine.

• Journal of Veterinary Clinics
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• v.18 no.1
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• pp.29-34
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• 2001

Antagonistic effects of atipamezole(50, 100, 200, 400 $\mu\textrm{g}$/kg, i.m.) on sedation induced with xylazine (2 mg/kg, i.m.) were evaluated in dogs. Atipamezole at doses of 100~400$\mu\textrm{g}$/kg effectively reversed sedation, and the arousal time, standing time and total recovery time were significantly shortened. The optimal action of atipamezole was seen at a dose of 100 $\mu\textrm{g}$/kg. At this dose recovery from sedation was quick and smooth, and adverse effects such as hyperactivity or tachycardia were minimal with or without atropine premedication.

• Journal of Veterinary Clinics
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• v.23 no.1
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• pp.18-21
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• 2006

This study was performed to investigate the reverse effects of atipamezole in green iguana anesthetized with intramuscular administration of medetomidine-tiletamine/zolazepam ($Zoletil^{\circledR}$). Heart rate, respiratory rate and body temperature were measured. Anesthetic depth was evaluated by righting reflex. In all study groups, heart rate and respiratory rate significantly decreased at 5 min after anesthetic administration, and gradually increased after atipamezole administration. The present study suggested that $500{\mu}g/kg$ atipamezole was effective reversal dosage for $500{\mu}g/kg$ medetomidine and 10 mg/kg liletamine/zolazepam combination anesthesia in green iguanas.

• Journal of Veterinary Clinics
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• v.28 no.2
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• pp.211-218
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• 2011

The aims of this study were to investigate the anesthetic effects of medetomidine-midazolam-ketamine (MMK) combination and to compare antagonistic effects of atipamezole and yohimbine in dogs anesthetized with MMK. Eighteen adult male healthy beagles were used in this study. All dogs were anesthetized with intramuscular (IM) administration of medetomidine (0.04 mg/kg), midazolam (0.2 mg/kg) and ketamine (5 mg/kg) in one syringe. Intravenous (IV) administration of atipamezole (0.24 mg/kg, MMKA), yohimbine (0.2 mg/kg, MMKY) or saline solution (0.1 ml/kg, MMK) was administered 20 minutes after MMK combination anesthesia. Induction and recovery times, scores of sedation and analgesia, heart rate, blood pressure, rectal temperature, respiratory rate and blood gases were determined and recorded for each dog. Mean anesthesia times, sternal recumbency times, standing times and walking times in the MMKA and MMKY groups were significantly shorter than those in the MMK group. But there were not significantly different between MMKA and MMKY groups. In all groups, MMK administration produced a satisfactory sedation and analgesia for all dogs. However, after administration of atipamezole or yohimbine the scores for posture and response to noxious stimuli were significantly lower in the MMKA or MMKY group than those in the MMK group. MMK produced good sedation and anesthesia effects, and atipamezole or yohimbine can be used as a safe and effective agent for antagonizing the MMK anesthesia in dogs.

• Journal of Veterinary Clinics
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• v.24 no.2
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• pp.104-108
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• 2007

The purpose of the study is to evaluate the clinical antagonistic effect of atipamezole(0.25 mg/kg, IM) in cats anesthetized with tiletamine-zolazepam ($Zoletil^{(R)}$, 10 mg/kg, IM) and medetomidine (0.05 mg/kg, IM). Twelve healthy 1 year old Korean mixed breed cats were used for this study. They were 4 males and 8 females. These cats were randomly assigned to two groups. One was control group ($Zoletil^{(R)}$ + medetomidine, ZM), and the other was treatment group ($Zoletil^{(R)}$ + medetomidine and antagonism by atipamezole, ZMA). All cats were examined 15 minutes before, 5, 25, 65 and 105 minutes after administration of tiletamine-zolazepam and medetomidine. Atipamezole was injected intramuscularly 20 minutes after ZM administation. Recovery time, heart rate, respiratory rate, total plasma protein and blood glucose were significantly different between ZM group and ZMA group (P<0.05). However, rectal temperature was not significantly different between ZM group and ZMA group. Two groups were able to induce sternal recumbency within 2 minutes and lateral recumbency within 4 minutes after the anesthetics injection. Mean sternal position time ($mean{\pm}SD$) was $174.0{\pm}44.6\;and\;116.2{\pm}27.3$ minutes, and mean standing position time was $210.8{\pm}45.6\;and\;154.2{\pm}21.1$ minutes in ZM and ZMA group, respectively. In these two groups, adverse effects during recovery time from anesthesia were not seen. As a result, the ZMA group had a faster recovery than the ZM group. Thus it was concluded that atipamezole could exert a useful reversal effect in cats anesthetized with medetomidine-tiletamine/zolazepam combination.

• Journal of Veterinary Clinics
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• v.18 no.3
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• pp.226-231
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• 2001

We investigated the effects of interactions of medetomidine and atipamezole on electroencephalography (EEG) in seven dogs. The dogs were sedated with medetomidine at dose of 30$\mu\textrm{g}$/kg, IM. Atipamezole was injected 15 min later at dose of 30$\mu\textrm{g}$/kg, IV. Recording electrode was positioned at Cz, which was applied to International 10-20 system. Heart rates, arterial blood pressures and behavioral changes were also measured. EEG was recorded in 6 stages(S1: before medetomidine injection, S2: prior to head-down movement after medetomidine injection, S3: 5 minutes after medetomidine injection, S4: 10 minutes after medetomidine injection, S5: 15 minutes after medetomidine injection, S6: prior to head-up movement after atipamezole injection), and heart rates and arterial pressures were recorded at S1, S5 and S6. All results were compared with those of control(S1). After medetomidine injection, the power spectra of EEG were gradually decreased and those of the frequency over 13 Hz were significantly decreased(p<0.05), which were still in the significantly decreased state after atipamezole injection. In the band powers (Band1; 1-2.5 Hz, Band2; 2.5-4.5 Hz, Band3; 4-8Hz, Band4; 8-13 Hz, Band5; 13-20 Hz, Band6; 20-30 Hz, Band7; 30-50 Hz, Band8; 1-50 Hz), band 1, 2, 3, 4, 8 were not significantly changed in any stages. Band 5, 6, 7 were significantly decreased in S 3, 4, 5, 6. That is, medetomidine affects the frequency band over 13 Hz on EEG, and atipamezole does not restored the decreased band powers until dogs showed head-up movement.

• Korean Journal of Veterinary Research
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• v.43 no.3
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• pp.501-505
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• 2003

The chemical immobilization in giraffes (Giraffa camelopardalis reticulata) remains a challenge because of their size, behavior, and anatomic and physiologic characteristics that commonly create life threatening problems during immobilization. The drug combination medetomidine (MED) and ketamine (KET) was administered by remote injection. The dosages of MED and KET were correlated to the giraffe's shoulder height (SH), become recumbent with a dosage of $114{\mu}g$ of MED and 2.1 mg of KET, $320{\mu}g$ of atipamezole per cm of SH, respectively. After injection of the drugs, initial signs of sedation including ataxia were noticed at 3 minutes followed by lateral recombency at 12 minutes. The mean heart rate, respiratory rate and rectal temperature recorded during the procedures were 55 beats per minute, 48 breaths per minute and $36.6^{\circ}C$, respectively. Atipamezole was administered, after 33 minutes result in death. Assuming that 24 hours fasting times were short and light esteemed of atipamzole adverse effects like vomiting, passive regurgitation.

• Journal of Veterinary Clinics
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• v.19 no.2
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• pp.174-185
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• 2002

We investigated the effects of yohimbine and atipamezole in dogs anesthetized with xylazine-ketamine combination on electroencephalography (EEG) . Experiment groups were divided into three according to antagonists . Saline (1 ml) was used as an antagonist in group C, yohimbine (0.1 mg/kg) in group Y and atipamezole (50 ug/kg) in group A. Each group consisted of 5 dogs. Glycopyrrolate was injected 15 minutes prior to xylazine injection. Xylazine (1.1 mg/kg, IM) and ketamime (10 mg/kg, IV) were injected with the interval of 10 minutes. After 15 minutes, antagonists were administered intravenously. For EEG measurements, a recording electrode was positioned at Cz, which was applied to International 10-20 system. Heart rates, body temperature, respiratory rates, arterial blood pressure, $PaO_2$$PaCO_2$$PaCO_2$ at S4 in group Y was significantly decreased(p<0.05). Changes of electrolytes were not significant, except value of $Cl^-$ at S3 in group A. Mean head-up time (the time dogs showing head-up movement after antagonist injection, minutes) was $38.23^{\circ}$ae6.46 in group C, 2.54 $\pm$ 0.93 in group Y and 2.12$\pm$ 1.32 in group A. Mean sternal recumbent time (the time dogs showing sternal recumbency after antagonist injection, minutes) was 45.93$\pm$ 10.27 in group C, 11.91 $\pm$ 7.19 in group Y and 9.88$\pm$ 3.38 in group A. Mean walking time (minutes) was 53.49$\pm$ 9.21 in group C, 22.10$\pm$ 11.10 in group Y and 18.48$\pm$ 4.39 in group A. In group Y all dogs showed excitation and muscle rigidity in emergence. In group A, two dogs were also showed excitation and muscle rigidity, but were weaker than those of group Y.

• The Korean Journal of Pain
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• v.27 no.4
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• pp.313-320
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• 2014

Dexmedetomidine, an imidazoline compound, is a highly selective ${\alpha}_2$-adrenoceptor agonist with sympatholytic, sedative, amnestic, and analgesic properties. In order to minimize the patients' pain and anxiety during minimally invasive spine surgery (MISS) when compared to conventional surgery under general anesthesia, an adequate conscious sedation (CS) or monitored anesthetic care (MAC) should be provided. Commonly used intravenous sedatives and hypnotics, such as midazolam and propofol, are not suitable for operations in a prone position due to undesired respiratory depression. Dexmedetomidine converges on an endogenous non-rapid eye movement (NREM) sleep-promoting pathway to exert its sedative effects. The great merit of dexmedetomidine for CS or MAC is the ability of the operator to recognize nerve damage during percutaneous endoscopic lumbar discectomy, a representative MISS. However, there are 2 shortcomings for dexmedetomidine in MISS: hypotension/bradycardia and delayed emergence. Its hypotension/bradycardiac effects can be prevented by ketamine intraoperatively. Using atipamezole (an ${\alpha}_2$-adrenoceptor antagonist) might allow doctors to control the rate of recovery from procedural sedation in the future. MAC, with other analgesics such as ketorolac and opioids, creates ideal conditions for MISS. In conclusion, dexmedetomidine provides a favorable surgical condition in patients receiving MISS in a prone position due to its unique properties of conscious sedation followed by unconscious hypnosis with analgesia. However, no respiratory depression occurs based on the dexmedetomidine-related endogenous sleep pathways involves the inhibition of the locus coeruleus in the pons, which facilitates VLPO firing in the anterior hypothalamus.