Antagonism of medetomidine sedation by atipamezole in pigs.

The efficacy of atipamezole as a medetomidine antagonist was evaluated in pigs. The atipamezole doses (intramuscularly) were 80, 160, 320 and 480 micrograms/kg of body weight, which were one, two, four and six times higher than the preceding medetomidine dose (80 micrograms/kg, intramuscularly). Atipamezole effectively reversed medetomidine-induced sedation, and the optimal action was seen at doses of 160 and 320 micrograms/kg. Recovery from sedation was quick and smooth, and adverse effects such as hyperactivity or tachycardia were minimal with either dose.     

Reversal of medetomidine-induced cardiovascular and respiratory changes with atipamezole in dogs

The effects of atipamezole, an alpha 2-antagonist, on six medetomidine-sedated laboratory beagles were studied in a randomised complete block design. The dogs were sedated with medetomidine (20, 40 or 80 micrograms/kg intramuscularly) and five- and 10-fold larger doses of atipamezole were administered intramuscularly 30 minutes later. Atipamezole significantly increased the medetomidine-depressed heart rate, respiratory frequency and arterial Po2. The drug also transiently decreased the mean arterial blood pressure but subsequently the blood pressure of the treated group did not differ from that of a group of dogs treated with a placebo.     

Reversal of medetomidine sedation by atipamezole in dogs

Atipamezole reversed the sedative effect of medetomidine in twelve laboratory beagles. The dogs were sedated with medetomidine doses of 20, 40 and 80 micrograms/kg body wt i.m. Atipamezole was injected (i.m.) 20 min later at dose rates two, four, six and ten times higher (in micrograms/kg) than the preceding medetomidine dose. Placebo treatment was included in the study. The deeply sedated dogs showed signs of arousal in 3-7 min and took their first steps 4-12 min after atipamezole injection. The dose-related reversal effect of atipamezole proved to be optimal with doses which were four, six or ten times higher than the preceding medetomidine dose. Drowsiness was found 0.5-1 h after atipamezole injection in 41% of the cases. No adverse effects nor cases of over-alertness or excitement were found.     

Clinical effectiveness of atipamezole as a medetomidine antagonist in cats

The efficacy of atipamezole to reverse medetomidine induced effects in cats was investigated in a clinical study (n=160) including placebo. The atipamezole doses (intramuscularly) were two, four and six times (2X, 4X and 6X) the preceding medetomidine dose, which was 100 ug/kg body weight intramuscularly. Medetomidine was shown to produce moderate to deep sedation, recumbency and bradycardia in cat. Atipamezole was clearly able to reverse these effects of medetomidine. The median arousal time in the atipamezole dose groups was five minutes and walking time, 10 minutes, compared with more than 30 minutes in the placebo group. Heart rate was increased towards normal by atipamezole in a dose related manner. The clinical evaluation of the ability of atipamezole to reverse the effects of medetomidine was found to be ‘good’ in 82-5, 75 or 65 per cent of cases in dose groups 2X, 4X and 6X, respectively. The effect of atipamezole was evaluated as being ‘too potent’ in 2–5, 5 or 25 per cent of the cases in these respective groups. The incidence of side effects was negligible. In conclusion, atipamezole at the dose of two to four times the preceding dose of medetomidine seems to be an effective medetomidine antagonist for clinical use in cats.     

Medetomidine, a new sedative-analgesic for use in the dog and its reversal with atipamezole

The sedative and physiological effects of intramuscular medetomidine (20 and 40 μg/kg) in dogs were compared with those of xylazine (2 mg/kg). The efficacy of atipamezole (200 μg/kg), as an antagonist given 15 or 45 minutes after medetomidine (40 μg/kg) was studied. Following medetomidine, onset of sedation was rapid, and depth and duration of sedation were dose dependent. The higher dose produced jaw relaxation, depression of the pedal reflex, downward rotation of the eye and dogs could be positioned for radiography of the hips. Side effects were similar after either medetomidine or xylazine, and included bradycardia, a fall in respiratory rate and muscle tremor. Vomiting during induction was less frequent after medetomidine than after xylazine. Intramuscular administration of atipamezole rapidly reversed the sedative effects of medetomidine. Signs of arousal were seen within three minutes; all dogs could stand within 10 minutes and appeared clinically normal. Heart and respiratory rates rose, but did not return to presedation values. Relapse to sedation was not noted.     

Antagonistic effects of atipamezole and yohimbine on medetomidine-induced diuresis in healthy dogs

This study aimed to investigate and compare the antagonistic effects of atipamezole and yohimbine on medetomidine-induced diuresis in healthy dogs. Five dogs were used repeatedly in each of 8 groups. One group was not medicated. Dogs in the other groups received 20 μg/kg of medetomidine intramuscularly and, 0.5 h later, saline (as the control injection), 50, 100, or 300 μg/kg of atipamezole, or 50, 100, or 300 μg/kg of yohimbine intramuscularly. Urine and blood samples were taken 11 times over 24 h for measurement of the following: urine volume, specific gravity, and creatinine concentration; urine and plasma osmolality; urine and plasma concentrations of electrolytes and arginine vasopressin (AVP); and the plasma concentration of atrial natriuretic peptide (ANP). Both atipamezole and yohimbine antagonized the diuretic effect of medetomidine, inhibiting medetomidine-induced decreases in urine specific gravity, osmolality, and concentrations of creatinine, sodium, potassium, chloride, and AVP and reversing both the medetomidine-induced increase in plasma concentrations of sodium, potassium, and chloride and the medetomidine-induced decrease in the plasma AVP concentration. Atipamezole significantly stimulated ANP release. The antidiuretic action of yohimbine was more potent than that of atipamezole but was not dose-dependent, in contrast to the action of atipamezole. The effects of these drugs may not be due only to actions mediated by α₂-adrenoceptors.     

The effect of medetomidine premedication upon propofol induction and infusion anaesthesia in the dog

The effect of premedication with four different intramuscular doses of medetomidine (5.0,10.0, 20.0 and 40.0 μg.kg-¹) and a saline placebo were compared in a group of six adult beagle dogs anaesthetised with propofol on five separate occasions. Anaesthesia was induced 30 minutes after premedication and maintained by intravenous injection and continuous infusion of propofol. The effects of medetomidine were reversed with atipamezole 30 minutes after anaesthetic induction. The marked synergistic effects of medetomidine with propofol were demonstrated by a dose related reduction in the induction and infusion requirements for a similar degree of anaesthesia. The effect appeared exponential in nature; lower medetomidine doses produced a disproportionately greater effect.
The maintenance of anaesthesia with propofol following a saline placebo or low doses of medetomidine proved to be difficult. Higher doses of medetomidine required less propofol for induction and infusion and allowed a more stable anaesthesia to be maintained. Propofol produced no statistically significant change in heart rate during infusion. Changes in respiratory rate were markedly group specific. A significant reduction in respiratory rate was seen in dogs given either 5 μg.kg- or 10 μ-g.kg-¹ medetomidine. No change was recorded in dogs given 20 /μg.kg-¹ medetomidine and a significant increase was seen in dogs given 40 μg.kg-¹ medetomidine. Recovery was monitored following the termination of propofol infusion after the reversal of medetomidine using atipamezole at five times the medetomidine dose. Recovery was slower for dogs given lower doses of medetomidine and consequently higher doses of propofol.     

The cardiovascular and respiratory effects of medetomidine and thiopentone anaesthesia in dogs breathing at an altitude of 1486 m

The purpose of this study was to evaluate the cardio-respiratory effects of the combination of medetomidine and thiopentone followed by reversal with atipamezole as a combination for anaesthesia in 10 healthy German Shepherd dogs breathing spontaneously in a room at an altitude of 1486 m above sea level with an ambient air pressure of 651 mmHg. After the placement of intravenous and intra-arterial catheters, baseline samples were collected. Medetomidine (0.010 mg/kg) was administered intravenously and blood pressure and heart rate were recorded every minute for 5 minutes. Thiopentone was then slowly administered until intubation conditions were ideal. An endotracheal tube was placed and the dogs breathed room air spontaneously. Blood pressure, pulse oximetry, respiratory and heart rate, capnography, blood gas analysis and arterial lactate were performed or recorded every 10 minutes for the duration of the trial. Thiopentone was administered to maintain anaesthesia. After 60 minutes, atipamezole (0.025 mg/kg) was given intramuscularly. Data were recorded for the next 30 minutes. A dose of 8.7 mg/kg of thiopentone was required to anaesthetise the dogs after the administration of 0.010 mg/kg of medetomidine. Heart rate decreased from 96.7 at baseline to 38.5 5 minutes after the administration of medetomidine (P < 0.05). Heart rate then increased with the administration of thiopentone to 103.2 (P < 0.05). Blood pressure increased from 169.4/86.2 mmHg to 253.2/143.0 mmHg 5 minutes after the administration of medetomidine (P < 0.05). Blood pressure then slowly returned towards normal. Heart rate and blood pressure returned to baseline values after the administration of atipamezole. Arterial oxygen tension decreased from baseline levels (84.1 mmHg) to 57.8 mmHg after the administration of medetomidine and thiopentone (P < 0.05). This was accompanied by arterial desaturation from 94.7 to 79.7% (P < 0.05). A decrease in respiratory rate from 71.8 bpm to 12.2 bpm was seen during the same period. Respiratory rates slowly increased over the next hour to 27.0 bpm and a further increases 51.4 bpm after the administration of atipamezole was seen (P < 0.05). This was maintained until the end of the observation period. Arterial oxygen tension slowly returned towards normal over the observation period. No significant changes in blood lactate were seen. No correlation was found between arterial saturation as determined by blood gas analysis and pulse oximetry. Recovery after the administration of atipamezole was rapid (5.9 minutes). In healthy dogs, anaesthesia can be maintained with a combination of medetomidine and thiopentone, significant anaesthetic sparing effects have been noted and recovery from anaesthesia is not unduly delayed. Hypoxaemia may be problematic. Appropriate monitoring should be done and oxygen supplementation and ventilatory support should be available. A poor correlation between SpO2 and SaO2 and ETCO2 and PaCO2 was found.     

The clinical effectiveness of atipamezole as a medetomidine antagonist in the dog

The efficacy of atipamezole, a recently introduced alpha 2-adrenoceptor antagonist, in reversing medetomidine-induced effects in dogs was investigated in a clinical study. Dogs from eight Finnish small-animal hospitals were sedated with a 40-microgram/kg dose of the alpha 2-agonist medetomidine i.m. In the first part of the study (n = 319), a randomized, double-blind design with respect to the dose of atipamezole (0, 80, 160 and 240 micrograms/kg i.m.) was used. In a separate study (n = 358), which was an open trial, the selected dose of atipamezole was 200 micrograms/kg i.m. Atipamezole at dose rates of 80-240 micrograms/kg rapidly and effectively reversed medetomidine-induced deep sedation-analgesia, recumbency and bradycardia. The median arousal time after atipamezole was 3-5 min, and walking time was 6-10 min compared to greater than 30 min for both effects after placebo. Heart rate also increased in a dose-related manner after atipamezole administration. The investigators' overall evaluation of the ability of atipamezole to reverse the effects of medetomidine was 'good' in 90%, and 'moderate' in 9% of cases. Relapse into sedation was reported in three individual cases. Side-effects were minimal. It is concluded that at doses four- to sixfold the medetomidine dose, atipamezole is a highly effective and safe agent in reversing medetomidine-induced sedation-analgesia, recumbency and bradycardia in dogs in veterinary practice.     

Effects of medetomidine on doppler variables of major abdominal arteries in normal dogs

The purpose of this study was to evaluate the effects of medetomidine administration on the Doppler variables of abdominal arteries. The study population consisted of 20 healthy dogs. The haemodynamic effects of the medetomidine were defined using Doppler variables of the abdominal aorta, renal arteries, cranial mesenteric artery and celiac artery. The dogs were monitored continuously and different measurements were performed before medetomidine injection, at 10, 40 and 80 minutes after medetomidine medication and after atipamezole administration. Changes in the characteristic Doppler spectra of different vessels were more marked in the abdominal aorta, in which a greater reverse flow was found. There was a significant decrease in peak systolic velocity (PSV), end diastolic velocity (EDV), and mean velocity (MV) at ten minutes in every vessel studied and this effect persisted until atipamezole administration. Pulsatility index (PI) increased significantly in the abdominal aorta at ten minutes and persisted during the study until atipamezole administration. Resistive index (RI) did not vary significantly in any vessel. A significant decrease was found in flow volume of the abdominal aorta, the cranial mesenteric artery and the celiac artery at ten minutes, persisting until atipamezole administration. We conclude that medetomidine can be a good sedative in aiding sonographic evaluation of RI in all the abdominal vessels studied. On the other hand, the changes in other Doppler variables suggest that medetomidine administration causes significant hemodynamic differences between sedated and non-sedated dogs.     

Seizures during medetomindine sedation and local anaesthesia in two dogs undergoing skin biopsy

Each of two dogs presented for multiple skin biopsies were sedated with intravenous medetomidine and lignocaine was injected subcutaneously to provide local anaesthesia for skin biopsy. One dog had a seizure during skin biopsy and again immediately following reversal of medetomidine with atipamezole. The other dog developed seizures 2 h following skin biopsy at which time the medetomidine was reversed with atipamezole. Both dogs were neurologically normal with no history of seizures prior to the procedure and remained neurologically normal for 14 weeks and 9 months, respectively, following the procedure. A drug interaction between the α₂-adrenergic agonist medetomidine and lignocaine is suspected and highlights the potential for seizures following the subcutaneous administration of relatively large doses of lignocaine under medetomidine sedation.     

An evaluation of the influence of medetomidine hydrochloride and atipamezole hydrochloride on the arrhythmogenic dose of epinephrine in dogs during halothane anesthesia.

Alterations in the arrhythmogenic dose of epinephrine (ADE) were determined following administration of medetomidine hydrochloride (750 micrograms/M2) and a saline placebo, or medetomidine hydrochloride (750 micrograms/M2), followed by specific medetomidine reversal agent, atipamezole hydrochloride (50 micrograms/kg) 20 min later, in halothane-anesthetized dogs (n = 6). ADE determinations were made prior to the administration of either treatment, 20 min and 4 h following medetomidine/saline or medetomidine/atipamezole administration. Epinephrine was infused for 3 min at increasing dose rates (2.5 and 5.0 micrograms/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached. The interinfusion interval was 20 min. There were no significant differences in the amount of epinephrine required to reach the arrhythmia criterion following the administration of either treatment. In addition, the ADE at each determination was not different between treatment groups. In this study, the administration of medetomidine to halothane-anesthetized dogs did not alter their arrhythmogenic response to infused epinephrine.     

Antagonistic activities of atipamezole, 4-aminopyridine and yohimbine against medetomidine/ketamine-induced anaesthesia in cats

The objectives of this trial were to determine the ability of atipamezole, 4-aminopyridine and yohimbine to reverse the anaesthetic effects of a combination of medetomidine and ketamine in cats. Forty healthy cats were anaesthetised with 80 micrograms/kg medetomidine combined with 5 mg/kg ketamine. Thirty minutes later atipamezole (200 or 500 micrograms/kg), 4-aminopyridine (500 or 1000 micrograms/kg) or yohimbine (250 or 500 micrograms/kg) were injected intramuscularly. The doses of antagonists were randomised, so that each dose was administered to five cats, and 10 cats were injected only with physiological saline. Atipamezole clearly reversed the anaesthesia and bradycardia induced by medetomidine and ketamine. The mean (+/- sd) arousal times were 28 (+/- 4.7), 5.8 (+/- 1.8) and 7 (+/- 2.1) minutes in the placebo group, and the groups receiving 200 and 500 micrograms/kg atipamezole, respectively. The heart rates of the cats receiving 200 micrograms/kg atipamezole rapidly returned to values close to the initial ones, but 15 minutes after the injection of 500 micrograms/kg atipamezole a significant tachycardia was observed. All the cats showed moderate signs of ataxia during the recovery period. A dose of 500 micrograms/kg yohimbine also clearly reversed the anaesthetic effects of medetomidine/ketamine but 250 micrograms/kg was not effective. The dose of 500 micrograms/kg allowed a smooth recovery with no particular side effects except for some signs of incomplete antagonism of the ketamine effects, ie, ataxia and muscular incoordination. With 4-aminopyridine there were no statistically significant effects on the recovery, or the heart and respiratory rates of the cats anaesthetised with medetomidine/ketamine.     

Field anaesthesia of leatherback sea turtles (Dermochelys coriacea)

Ten nesting leatherback sea turtles on Trinidad were anaesthetised for electroretinogram (ERG) measurements, using ketamine and medetomidine, reversed with atipamezole. They weighed 242 to 324 kg and were given initial doses of 3 to 8 mg/kg ketamine and 30 to 80 microg/kg medetomidine administered into an external jugular vein; six of the turtles received supplementary doses of 2.6 to 3.9 mg/kg ketamine combined with 0 to 39 microg/kg medetomidine. The lower doses were used initially to ensure against overdosage and reduce the chances of residual effects after the turtles returned to the water, but successful ergs called for step-wise dose increases to the required level of anaesthesia. Respiratory rate, heart rate, electrocardiogram, cloacal temperature, and venous blood gases were monitored, and blood was collected for plasma biochemistry. At the end of the erg procedure, atipamezole was administered at 150 to 420 microg/kg (five times the dose of medetomidine), half intramuscularly and half intravascularly. The turtles were monitored and prevented from re-entering the water until their behaviour was normal. No apparent mortalities or serious anaesthetic complications occurred. The observed within-season return nesting rate of the anaesthetised turtles was comparable with that of unanaesthetised turtles.     

Effects of combinations of medetomidine/pethidine when used for sedation and pre-anaesthetic medication in dogs

Medetomidine, either 5, 10 or 20 (μg/kg, was administered together with pethidine, 2 mg/kg, by either the intramuscular or subcutaneous route to 88 dogs from a clinical population. Administration of all the drug combinations consistently produced profound sedation in the dogs, accompanied by dramatic reductions in heart rate. The degree of sedation was similar to that seen after 40 μg/kg medetomidine is administered on its own to dogs. Intramuscular administration produced more reliable sedation, but was associated with more pain than subcutaneous administration. In a number of dogs, sedation permitted the completion of various diagnostic or therapeutic procedures. Several dogs were anaesthetised with thiopentone and the induction doses required were characteristically low (mean doses between 2 to 3·3 mg/kg depending on the dose of medetomidine and the route of administration). Administration of atipamezole at the termination of sedation or anaesthesia, produced a rapid and full recovery (mean time to standing between seven and 11 minutes).     

Comparison of medetomidine and dexmedetomidine as premedicants in dogs undergoing propofol-isoflurane anesthesia.

OBJECTIVE: To compare 3 dose levels of medetomidine and dexmedetomidine for use as premedicants in dogs undergoing propofol-isoflurane anesthesia. ANIMALS: 6 healthy Beagles. PROCEDURE: Dogs received medetomidine or dexmedetomidine intravenously at the following dose levels: 0.4 microg of medetomidine or 0.2 microg of dexmedetomidine/kg of body weight (M0.4/D0.2), 4.0 microg of medetomidine or 2.0 microg of dexmedetomidine/kg (M4/D2), and 40 microg of medetomidine or 20 microg of dexmedetomidine/kg (M40/D20). Sedation and analgesia were scored before induction. Anesthesia was induced with propofol and maintained with isoflurane. End-tidal isoflurane concentration, heart rate, and arterial blood pressures and gases were measured. RESULTS: Degrees of sedation and analgesia were significantly affected by dose level but not drug. Combined mean end-tidal isoflurane concentration for all dose levels was higher in dogs that received medetomidine, compared with dexmedetomidine. Recovery time was significantly prolonged in dogs treated at the M40/D20 dose level, compared with the other dose levels. After induction, blood pressure decreased below reference range and heart rate increased in dogs treated at the M0.4/D0.2 dose level, whereas blood pressure was preserved in dogs treated at the M40/D20 dose level. However, dogs in these latter groups developed profound bradycardia and mild metabolic acidosis during anesthesia. Treatment at the M4/D2 dose level resulted in more stable cardiovascular effects, compared with the other dose levels. In addition, PaCO2 was similar among dose levels. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine is at least as safe and effective as medetomidine for use as a premedicant in dogs undergoing propofol-isoflurane anesthesia.     

Effect of medetomidine and its antagonism with atipamezole on stress-related hormones, metabolites, physiologic responses, sedation, and mechanical threshold in goats

OBJECTIVE: To evaluate the effects of medetomidine and its antagonism with atipamezole in goats. STUDY DESIGN: Prospective randomized crossover study with 1 week between treatments. ANIMALS: Six healthy 3-year-old neutered goats (three male and three female) weighing 39.1-90.9 kg (60.0 +/- 18 kg, mean +/- SD). METHODS: Goats were given medetomidine (20 microg kg(-1), IV) followed, 25 minutes later, by either atipamezole (100 microg kg(-1), IV) or saline. Heart and respiratory rate, rectal temperature, indirect blood pressure, and mechanical threshold were measured, and sedation and posture were scored and blood samples obtained to measure epinephrine, norepinephrine, free fatty acids, glucose, and cortisol concentrations at baseline (immediately before medetomidine), 5 and 25 minutes after medetomidine administration, and at 5, 30, 60, and 120 minutes after the administration of antagonist or saline. Parametric and nonparametric tests were used to evaluate data; p < 0.05 was considered significant. RESULTS: Medetomidine decreased body temperature, heart rate, and respiratory rate and increased mean arterial blood pressure, cortisol, and glucose. Recumbency occurred 89 +/- 50 seconds after medetomidine administration. All goats were standing 86 +/- 24 seconds after atipamezole administration whereas all goats administered saline were sedate and recumbent at 2 hours. Tolerance to compression of the withers and metacarpus increased with medetomidine. From 5 to 120 minutes after saline or atipamezole administration, there were differences in body temperature, glucose, and cortisol but none in heart rate or blood pressure. Three of the six goats receiving saline developed bloat; five of six urinated. After atipamezole, four of six goats developed piloerection and all goats were agitated and vocalized. CONCLUSION: At the doses used, atipamezole antagonized the effects of medetomidine on recumbency, sedation, mechanical threshold, and the increase in glucose. Atipamezole increased the rate of return of cortisol toward baseline, and prevented further decline in rectal body temperature. CLINICAL RELEVANCE: Atipamezole may be used to antagonize some, but not all effects of medetomidine.     

Evaluation of the clinical efficacy and safety of dexmedetomidine or medetomidine in cats and their reversal with atipamezole

OBJECTIVE: To evaluate and compare the clinical effects of dexmedetomidine (DEX) and medetomidine (MED) in cats, and their reversal with atipamezole (ATI). Study design Prospective blinded randomized multi-centre clinical trial. Animals One hundred and twenty client-owned cats. METHODS: Cats were randomly allocated to receive a single intramuscular (IM) injection of either DEX (0.04 mg kg(-1), n = 62) or MED (0.08 mg kg(-1), n = 58) for minor procedures requiring sedation and analgesia. Afterwards, ATI (0.2 mg kg(-1)) was administered IM to half the cats, randomly assigned. Prior to, during and after the procedure the sedative, analgesic and cardiorespiratory effects and body temperature were assessed. RESULTS: Dexmedetomidine and MED produced clinically and statistically comparable effects. The intended procedure(s) could be performed in over 90% of cats. Sedation and analgesia were apparent within 5 minutes, peak effects were observed at approximately 30 minutes and spontaneous recovery occurred by 180 minutes of injection. Heart and respiratory rate and body temperature decreased significantly over time and had not returned to baseline values 180 minutes after administration. ATI administration completely reversed the sedative and analgesic effects, returned the heart rate to normal and prevented any further reductions in respiratory rate and body temperature in both DEX- and MED-treated cats. The reporting of adverse events was low and the most commonly observed event was vomiting (7%). No serious adverse events or concerns regarding safety were reported. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine (0.04 mg kg(-1)) produced comparable sedative and analgesic effects to MED (0.08 mg kg(-1)) in cats. DEX produced adequate sedation and analgesia for radiography, grooming, dental care and lancing of abscesses. ATI fully reversed the clinical effects of DEX.     

Medetomidine/ketamine sedation in calves and its reversal with atipamezole

Atipamezole was used to reverse the sedation induced in calves by medetomidine/ketamine. Thirteen claves subjected to umbilical surgery received medetomidine 20 μg/kg bodyweight (bwt) and ketamine 0.5 mg/kg bwt intravenously (iv) from a mixture of the drugs in one syringe. Atipamezole was given at doses of 20 to 60 μg/kg iv and intramuscularly (im) to the calves at the end of the operation. Following the administration of medetomidine and ketamine, PaCO₂ increased whereas pH, PaO₂ and heart rate decreased. Reversing the effects of medetomidine with atipamezole did not cause undesirable effects; recovery was rapid and smooth, most of the animals reached a standing position within 1 to 3 mins after the atipamezole injection.     

Effects of medetomidine and medetomidine-butorphanol combination on Schirmer tear test 1 readings in dogs

Medetomidine is a commonly used sedative in veterinary medicine whether administered alone or in combination with an opioid such as butorphanol. There are no previous studies that look at the effects of this drug on sequential Schirmer tear test (STT) 1 readings in dogs, including effects on tear production after reversal of the drug. The present study looked at two groups of 10 dogs each that were sedated with intravenous medetomidine or a combination of medetomidine and butorphanol. All dogs had tear readings taken presedation, 15 min postsedation, and 15 min after reversal of medetomidine with atipamezole. Results revealed that intravenous sedation with medetomidine and medetomidine-butorphanol in dogs with no history of ophthalmic disease and presedation STT 1 readings above 15 mm/min, causes a significant decrease in tear production that is measurable at 15 min postsedation. Readings returned to near presedation values within 15 min postreversal in most cases. It is therefore recommended that all eyes be treated with a tear substitute from the time the sedative is given until at least 15 min after reversal.