Effects Of Medetomidine Research Articles

Effect of medetomidine with or without vatinoxan on some ocular variables in healthy dogs

Effect of medetomidine with or without vatinoxan on some ocular variables in healthy dogs

Comparison of the sedative and cardiovascular effects of medetomidine and medetomidine-vatinoxan, combined with butorphanol, in pediatric dogs undergoing brainstem auditory-evoked response testing

Comparison of the sedative and cardiovascular effects of medetomidine and medetomidine-vatinoxan, combined with butorphanol, in pediatric dogs undergoing brainstem auditory-evoked response testing

Comparing the cardiovascular and sedative effects of medetomidine and vatinoxan hydrochloride with dexmedetomidine in dogs undergoing official hip radiography

Comparing the cardiovascular and sedative effects of medetomidine and vatinoxan hydrochloride with dexmedetomidine in dogs undergoing official hip radiography

Comparative evaluation of the intravenous effect of medetomidine, tramadol and medetomidine/tramadol combination on tear production in clinically healthy donkeys (Equus asinus)

Various ophthalmic disorders (conjunctivitis, corneal wounds, keratitis) have been reported in donkeys. There are no studies on the effect of medetomidine or tramadol on Schirmer tear test (STT) readings in donkeys. This prospective study investigated changes in STT readings in 24 clinically healthy donkeys (Equus asinus) (14 geldings and 10 mares) treated with commonly used doses of medetomidine hydrochloride and tramadol hydrochloride as mono- or combined therapy. Analgesia, sedation, ataxia, and STT readings were measured before treatment (baseline) and at different periods after administration (5–120 min) of the specific drug in each group. Tramadol monotherapy induced a mild analgesic effect (score 1) at 10 min post-administration. All treated donkeys exhibited mild to moderate ataxia. Medetomidine alone or in combination with tramadol induced a significant decrease (P<0.05) in the STT readings in both right and left eyes at 5, 15, 30, and 60 min relative to baseline, and the lowest values were observed 60 min after drug administration in both groups. Intravenous administration of medetomidine alone or in combination with tramadol induced a significant reduction in STT readings in clinically healthy donkeys. Therefore, in donkeys, the ocular surface treated with these sedatives should be carefully examined and adequately covered by an artificial tear solution or ophthalmic gel.

Efficacy and safety of three different opioid-based immobilisation combinations in blesbok (Damaliscus pygargus phillipsi).

African wildlife species are increasingly being immobilised with combinations of a low dose of potent opioids combined with medetomidine and azaperone. The physiological effects of these combinations in comparison to conventional potent opioidazaperone combinations have scarcely been evaluated. In this cross-over study conducted on eight captive blesbok, we compared the physiological variables of blesbok immobilised with 2 mg of thiafentanil + 10 mg of azaperone (TA); 0.5 mg thiafentanil + 1.5 mg medetomidine (TM), and 0.5 mg thiafentanil + 1.5. mg medetomidine + 10 mg azaperone (TMA). Thiafentanil's effects were antagonised with naltrexone at 10 mg naltrexone per mg thiafentanil, and the medetomidine effects with atipamezole at 5 mg atipamezole per mg medetomidine. The physiological variables were compared between treatment groups using descriptive statistics and repeated measures ANOVA. The TA combination resulted in the shortest induction and recovery times, higher heart rates, respiratory rates, PaO2, SpO2, and lower MAP and A-a gradients, but with less muscle relaxation. The TM and TMA combinations caused marked bradycardia and hypoxaemia. The hypoxaemia was most severe in animals immobilised with TMA, and four of eight blesbok immobilised had a PaO2 < 35 mmHg at the 10- or 15-minute sampling point. These blesbok were provided supplementary oxygen, which corrected the hypoxaemia. The TA combinations caused the lowest degree of physiological compromise. All three combinations were effective for the immobilisation of blesbok, but as the low-dose thiafentanil and high-dose medetomidine combinations caused marked hypoxaemia, supplementary oxygen is recommended when using these combinations.

Evaluation of the Effects of Medetomidine and Dexmedetomidine Use on Intraocular Pressure in Cats

Evaluation of the Effects of Medetomidine and Dexmedetomidine Use on Intraocular Pressure in Cats

Effect of medetomidine, an anesthetic for animals, and dexmedetomidine, a sedative for humans, on thrombus formation.

Effect of medetomidine, an anesthetic for animals, and dexmedetomidine, a sedative for humans, on thrombus formation.

Effects of medetomidine and dexmedetomidine on intraocular pressure, pupil size, and tear secretion in clinically normal Ghezel sheep

The objectives of the study were to investigate the effects of dexmedetomidine and medetomidine on intraocular pressure (IOP), pupil size (PS), and tear secretion (TS) in sheep. A total of sixteen female Ghezel sheep aged 24 ± 6 months (mean + standard deviation) and weighing 54.3 ± 8.9 kg (mean ± standard deviation) were randomly selected for the experimental study. Sheep were randomly divided into two groups consisting of Dex (5 μg/kg dexmedetomidine, intravenously), and group Med (10 μg/kg medetomidine, intravenously) with eight animals in each group. The IOP, PS, and TS were measured before drug administration (T0), and after the drug administration at 15-minute intervals for 45 min (T15, T30, and T45). The mean IOP, PS, and TS values at T0 between the right and left eyes showed no significant differences (P = 0.83, P = 0.23 and P = 0.45, respectively). The IOP and TS were significantly decreased in both groups compared to baseline (P < 0.05). Although PS decreased in both groups, the reduction was not statistically significant (P > 0.05). For IOP, PS, and TS at any time point, there was no significant difference between the two groups (P > 0.05). In sheep, dexmedetomidine and medetomidine administration decreased the IOP and TS, whereas no significant alterations were observed in PS.

Comparative evaluation of the sedative and physiological effects of medetomidine alone and in combination with pethidine, morphine, tramadol, and methadone in goats.

BackgroundThe use of combinations of α2‐adrenergic agonists and opioids has been published as providing superior sedation than either drug alone.IntroductionThe present study aims to compare the sedative and physiological effects of intravenous (IV) administration of medetomidine alone and in combination with methadone, morphine, tramadol, and pethidine in goats.MethodsTen healthy goats aged 12 ± 3 months and weight of 22 ± 4 kg were used in an experimental, crossover (Latin square), randomized, and blinded study. The animals were assigned to five IV treatments with a minimum washout period of 8 days between treatments: medetomidine (20 μg kg−1), medetomidine/methadone (0.5 mg kg−1), medetomidine/morphine (0.5 mg kg−1), medetomidine/tramadol (5 mg kg−1), and medetomidine/pethidine (1 mg kg−1).ResultsClinical adverse effects such as tremors (facial and generalized), bruxism, nystagmus, mydriasis, and vocalization were presented in all the medetomidine/opioid treatments. Clinical adverse effects were observed at 10–90 minutes in medetomidine/opioid treatments. Animals in all treatments were sedated at 5–90 minutes. Sedation was significantly higher in medetomidine/opioid treatments than in medetomidine at 15–30 minutes after administration (P < 0.05). In all treatments, heart rate and respiratory rate significantly decreased from baseline at 5–105 and 30–60 minutes, respectively. There was no significant difference in heart and respiratory rates between different treatments at any time point. Ruminal motility was decreased in medetomidine and medetomidine/opioid treatments at 10–75 and 10–105 minutes, respectively. Compared with medetomidine, ruminal motility was significantly lower in medetomidine/opioid treatments at 75–105 minutes.ConclusionThe use of combinations of medetomidine/opioids would be considered for superior sedation at 15–30 minutes after administration in goats. No significant differences were detected among opioids in combination with medetomidine in goats.

Vatinoxan: a new development in the clinical use of α2-adrenoceptor agonists in dogs, part 1

Vatinoxan, formerly known as MK-467 or L-659 066, is a peripherally acting α2 adrenoceptor antagonist. In a similar manner to atipamezole, it antagonises the pharmacodynamic effects of the α2 adrenoceptor agonist medetomidine and its active enantiomer dexmedetomidine. However, unlike atipamezole it has limited ability to penetrate the blood–brain barrier, owing to its relatively low lipid solubility. Medetomidine is an α2 adrenoceptor agonist, which is commonly used in dogs because it is a profound and consistent sedative. However, its use is also associated with many side effects, most notably those affecting the cardiovascular system, which include but are not limited to vasoconstriction, hypertension and bradycardia. When vatinoxan is co-administered intravenously with medetomidine or dexmedetomidine, it has minimal impact on the quality of sedation but vatinoxan attenuates the cardiovascular effects of medetomidine and dexmedetomidine. By ameliorating the cardiovascular effects of the agonist drugs, vatinoxan alters their pharmacokinetics, thereby shortening their duration of effect. Following intramuscular injection, vatinoxan hastens the onset of sedation and its use is associated with a greater level but a shorter duration of sedation. Therefore, vatinoxan may offer some clinically beneficial effects when it is part of a sedative drug combination or when used for premedication before general anaesthesia in dogs.

Fasting prevents medetomidine-induced hyperglycaemia and alterations of neurovascular coupling in the somatosensory cortex of the rat during noxious stimulation.

Medetomidine and isoflurane are commonly used for general anaesthesia in fMRI studies, but they alter cerebral blood flow (CBF) regulation and neurovascular coupling (NVC). In addition, medetomidine induces hypoinsulinemia and hyperglycaemia, which also alter CBF regulation and NVC. Furthermore, sudden changes in arterial pressure induced by noxious stimulation may affect NVC differently under medetomidine and isoflurane anaesthesia, considering their different effects on vascular functions. The first objective of this study was to compare NVC under medetomidine and isoflurane anaesthesia during noxious stimulation. The second objective was to examine whether fasting may improve NVC by reducing medetomidine-induced hyperglycaemia. In male Wister rats, noxious electrical stimulation was applied to the sciatic nerve in fasted or non-fasted animals. CBF and local field potentials (LFP) were recorded in the somatosensory cortex to assess NVC (CBF/LFP ratio). The CBF/LFP ratio was increased by medetomidine compared with isoflurane (p = 0.004), but this effect was abolished by fasting (p = 0.8). Accordingly, medetomidine produced a threefold increase in blood glucose (p < 0.001), but this effect was also abolished by fasting (p = 0.3). This indicates that isoflurane and medetomidine anaesthesia alter NVC differently, but the undesirable glucose dependent effects of medetomidine on NVC can be prevented by fasting.

Evaluation of Medetomidine-Ketamine for Immobilization of Feral Horses in Romania.

Feral horses are immobilized for a variety of reasons including population control via contraceptives. Although opioid combinations have been successfully used for immobilization of feral horses, there is a need for combinations using drugs that are more readily available and present less of a human health hazard. We evaluated the chemical immobilization with physiological measurements and blood gas analyses of 91 free-ranging feral horses (Equus ferus caballus) remotely immobilized with a combination of 30 mg medetomidine and 775 mg ketamine in a single disposable 6 ml dart. During immobilization, heart rate, respiratory rate, rectal temperature, capillary refill time and peripheral oxygen hemoglobin saturation (SpO2) were evaluated. In eight horses, arterial blood samples were analyzed to evaluate the blood gases, acid-base status and hematologic variables. Targeted horses presented a wide range of age, size and body condition. Eighty-one horses had an uneventful mean induction of 7.2 min. Eighty-nine horses were immobilized in lateral recumbency with good muscle relaxation and a median recumbency time of 67 min. Ten horses required supplemental ketamine intravenously (x̄ = 434 mg) due to incomplete immobilization. In 58 horses the effects of medetomidine were antagonized with atipamezole intravenously. Increased respiratory rate (>20 breaths/min), increased heart rate (>45 beats/min) and decreased SpO2 < 90% were noted in more than half of the individuals, while increased rectal temperature (>39.0°C) was recorded in six animals. Blood parameters showed hypoxemia (<90 mmHg, n = 8), hypercapnia (>45 mmHg, n = 5), high glucose levels (>134 mmol/L, n = 3), increased blood lactate (>1.5 mmol/L), total carbon dioxide, bicarbonate and base excess which further increased in the second sample, whereas SpO2 and calcium values decreased. Recoveries were smooth, with one (n = 86) or more (n = 5) attempts of standing. Eighty-nine recoveries were uneventful, besides one male that showed signs of monoparesis of the left front leg and one mare with signs consistent with exertional myopathy. In conclusion, medetomidine-ketamine provided a reliable immobilization in feral horses over a wide range of body mass and age. However, based on the observed hypoxemia during immobilization, oxygen supplementation is strongly recommended for this protocol.

Disentanglement of Cape fur seals (Arctocephalus pusillus pusillus) with reversible medetomidine-midazolam-butorphanol.

Anaesthesia in pinnipeds is considered a much higher risk than in most terrestrial mammals because of their frequent proximity to water and physiological and anatomical adaptations related to diving, which also influence their anaesthesia management. Anaesthetising and immobilising entangled seals does not allow for selection of animals that are at a safe distance from the water’s edge. Medetomidine-midazolam-butorphanol (MMB) sedation was trialled on eight entangled Cape fur seals (CFS) (Arctocephalus pusillus pusillus) to determine if it was safe to use on animals that entered the water post-darting. The MMB was given at an estimated dose of 0.03 mg/kg, 0.2 mg/kg and 0.2 mg/kg, respectively, via remote darting. Sedation was reversed with intramuscular atipamezole (0.15 mg/kg) and naltrexone (0.4 mg/kg) to antagonise the effects of medetomidine and butorphanol, respectively. Moderate sedation was achieved in six animals. Six of the animals entered the water after being darted. There was a single mortality and a single animal that was too lightly sedated for capture. The preliminary results indicate that MMB produces suitable sedation for disentanglement of CFS. Additionally, MMB might be suitable for application to field-based biological research.

Effects of Medetomidine, Dexmedetomidine and their combination with Acepromazine on the intraocular pressure (IOP), tear secretion and pupil diameter in dogs

BackgroundA great number of sedatives and anaesthetics have been used to perform surgeries or routine ophthalmologic examinations in animals and sometimes the combination of these medicines has more suitable effects than each one alone.ObjectivesThis paper aims to explore the main effects of Medetomidine + Acepromazine, Dexmedetomidine + Acepromazine on intraocular pressure, tear secretion and pupil diameter.MethodsTo accomplish the aforementioned aim, 32 adult dogs (aged one‐to‐three‐years‐old) were clinically examined. Dogs were divided into four groups consisting of group DA, Dexmedetomidine (5 µg/kg) + Acepromazine (0.05 mg/kg); Group D, Dexmedetomidine (5 µg/kg); Group M, Medetomidine (10 µg/kg); Group MA, Medetomidine (10 µg/kg) + Acepromazine (0.05 mg/kg). The ocular factors including tear production, pupil diameter and intraocular pressure of both right and left eyes were first measured and then recorded in each dog at time T0 (−15 min). Afterwards, the drugs were administered intramuscularly, based on which the ocular factors were re‐measured at T1 (+5 min), T2 (+15 min) and T3 (+20 min). All four groups showed a reduction in intraocular pressure, which was significant in DA, D and M groups.ResultsFurthermore, there was a fluctuation in the amount of tear secretion in DA and D groups (increase and then decrease), as well as a significant reduction in M and MA groups. Decreasing in pupil diameter also occurred in all four groups, but the reduction was significant only in DA and MA groups.ConclusionAccording to the results obtained, as the changes caused by the systemic administration of the above drug compounds did not exceed the physiological range, it can be concluded that these combinations could be utilized as suitable sedatives or pre‐anaesthetic compounds in the eye surgeries.

Effect of medetomidine on left ventricular outflow tract velocity in cats: A Doppler echocardiography study.

The purpose of the present study was to evaluate effects of medetomidine on left ventricular outflow tract (LVOT) velocity in domestic short-haired cats. Eighteen healthy adult male domestic short-haired cats were used for this study. All animals were client-owned. Echocardiography machine with 7.50 MHz transducer was used. Specific veterinary two-dimensional and pulse-waved echocardiogram images in apical five chamber right parasternal view were obtained and blood velocity in LVOT was calculated. After baseline echocardiographic recordings, 0.04 mg kg-1 of medetomidine was intramuscularly administered to each animal and LVOT velocity was calculated after 15 (T15), 50 (T30) and 80 (T80) min following drug administration. The LVOT velocity values (mean SEM) of cats in baseline were 1.06 0.04 m sec-1. There were significant differences between baseline and T15 and T30 regarding mean LVOT values. Age and weight had no significant effect on LVOT velocity values. The LVOT velocity values of T15, T50 and T80 were 0.77 0.04, 0.80 0.02 and 0.960.03 m sec-1, respectively. Our findings revealed significant decrease in mean LVOT velocity up to 50 min following medetomidine administration. The present study determined normal LVOT velocity range for a small population of cats before and after intra-muscular medetomidine administration.

Effect of Medetomidine, Dexmedetomidine, and Their Reversal with Atipamezole on the Nociceptive Withdrawal Reflex in Beagles.

Simple SummaryMedetomidine, an alpha-2 agonist routinely used to provide sedation and pain relief in dogs, is a mixture of dexmedetomidine and levomedetomidine in equal proportions. Dexmedetomidine, considered to be the only active component in the mixture, is also marketed alone. Sedation caused by both formulations can be reversed using atipamezole, which shortens recovery. Dexmedetomidine provides analgesic effects similar to medetomidine, but it remains unclear at which dose and whether the analgesic effects of medetomidine or dexmedetomidine disappear once atipamezole is injected. The present trial aimed at elucidating these uncertainties using the nociceptive withdrawal reflex model. This model allows for quantification of analgesia by measuring specific activity from muscles involved in limb withdrawal in response to mild electrical stimulation. In eight beagles, the model was applied to compare the extent of pain relief provided by medetomidine and dexmedetomidine and to investigate whether complete reversal occurs after the administration of atipamezole. No difference in analgesic efficacy was identified between the two formulations. Both sedation and pain relief terminated rapidly when atipamezole was administered. These findings indicate that medetomidine and dexmedetomidine provide comparable levels of pain relief and that additional analgesics may be necessary when atipamezole is administered to dogs experiencing pain.The objectives were: (1) to compare the antinociceptive activity of dexmedetomidine and medetomidine, and (2) to investigate its modulation by atipamezole. This prospective, randomized, blinded experimental trial was carried out on eight beagles. During the first session, dogs received either medetomidine (MED) (0.02 mg kg−1 intravenously (IV)] or dexmedetomidine (DEX) [0.01 mg kg−1 IV), followed by either atipamezole (ATI) (0.1 mg kg−1) or an equivalent volume of saline (SAL) administered intramuscularly 45 min later. The opposite treatments were administered in a second session 10–14 days later. The nociceptive withdrawal reflex (NWR) threshold was determined using a continuous tracking approach. Sedation was scored (0 to 21) every 10 min. Both drugs (MED and DEX) increased the NWR thresholds significantly up to 5.0 (3.7–5.9) and 4.4 (3.9–4.8) times the baseline (p = 0.547), at seven (3–11) and six (4–9) minutes (p = 0.938), respectively. Sedation scores were not different between MED and DEX during the first 45 min (15 (12–17), p = 0.67). Atipamezole antagonized sedation within 25 (15–25) minutes (p = 0.008) and antinociception within five (3–6) minutes (p = 0.008). Following atipamezole, additional analgesics may be needed to maintain pain relief.

Effects of Sedation by Intramuscular Administration of Medetomidine on Canine Abdominal Vascular System and Hepatic Parenchyma Imaging Using Enhancement Dynamic Computed Tomography

This prospective crossover study compared the effects of intramuscular administration of medetomidine for sedation on parameters of the abdominal vascular system, measured by enhancement computed tomography (CT), to those of propofol-induced sevoflurane maintenance anesthesia, as a control, in five clinically healthy adult male beagle dogs (11.4–12.8 kg). Each animal underwent both protocols at a 1-week interval. The enhancement (HU) and time to peak enhancement on CT were measured for the aorta (AO), caudal vena cava (CVC), portal vein (PV), and hepatic parenchyma (HP). The contrast effects in the AO, PV, and HP were significantly delayed under medetomidine sedation compared to the control anesthesia protocol. Particularly, the contrast effect in the PV and HP was significantly delayed under sedation, appearing approximately 1 min after contrast medium injection. This delay likely reflects the peripheral vasoconstrictive effect of medetomidine. We noted a generally early high contrast enhancement of the CVC under medetomidine sedation, likely contributed by the induced bradycardia. Therefore, findings obtained on contrast enhancement CT under medetomidine sedation may be different from those obtained under propofol-induced sevoflurane maintenance anesthesia. These differences are important to consider when using the findings to inform diagnosis.

Effect of Intramuscular Medetomidine Administration on Tear Flow in Rats.

Medetomidine has been reported to decrease tear flow significantly in dogs, cats, and pigs when used as a sedative or analgesic; however, there are no such reports when it comes to rats. The present study aimed to investigate the effect of medetomidine on tear flow in rats. Medetomidine in doses of 50, 100, or 200 µg/kg or a physiological saline solution as the control, were administered intramuscularly to male Slc:Wistar/ST rats. After the administration of medetomidine, tear flow in both eyes was measured using a phenol red thread tear test. The area under the curve (AUC) of phenol red thread test values from baseline to 8 h was calculated. Data were plotted against the dose of medetomidine and simple linear regression analysis was performed. The effect of the drug on phenol red thread test values was considered dose-related when linear analysis yielded a significant relationship. In all medetomidine-treated groups, tear flow decreased significantly in both eyes after administration, while no significant changes were observed in either eye in the control group. The AUC values from baseline to 8 h after administration in groups treated with 100 and 200 µg/kg of medetomidine were significantly lower in both the left and right eyes compared to the control group. The linear regression of the AUC values was significant for both eyes. Our results indicated that the intramuscular administration of medetomidine in rats decreased tear flow significantly in a dose-dependent manner.

Investigation of the effects of vatinoxan on somatic and visceral antinociceptive efficacy of medetomidine in dogs

To determine whether concurrent vatinoxan administration affects the antinociceptive efficacy of medetomidine in dogs at doses that provide circulating dexmedetomidine concentrations similar to those produced by medetomidine alone. 8 healthy Beagles. Dogs received 3 IV treatments in a randomized crossover-design trial with a 2-week washout period between experiments (medetomidine [20 μg/kg], medetomidine [20 μg/kg] and vatinoxan [400 μg/kg], and medetomidine [40 μg/kg] and vatinoxan [800 μg/kg]; M20, M20V400, and M40V800, respectively). Sedation, visceral and somatic nociception, and plasma drug concentrations were assessed. Somatic and visceral nociception measurements and sedation scores were compared among treatments and over time. Sedation, visceral antinociception, and somatic antinociception effects of M20V400 and M40V800 were analyzed for noninferiority to effects of M20, and plasma drug concentration data were assessed for equivalence between treatments. Plasma dexmedetomidine concentrations after administration of M20 and M40V800 were equivalent. Sedation scores, visceral nociception measurements, and somatic nociception measurements did not differ significantly among treatments within time points. Overall sedative effects of M20V400 and M40V800 and visceral antinociceptive effects of M40V800 were noninferior to those produced by M20. Somatic antinociception effects of M20V400 at 10 minutes and M40V800 at 10 and 55 minutes after injection were noninferior to those produced by M20. Results suggested coadministration with vatinoxan did not substantially diminish visceral antinociceptive effects of medetomidine when plasma dexmedetomidine concentrations were equivalent to those produced by medetomidine alone. For somatic antinociception, noninferiority of treatments was detected at some time points.

Comparison of the sedative effects of medetomidine administered intranasally, by atomization or drops, and intramuscular injection in dogs

ObjectiveTo compare the sedative effects of intranasal atomization (INA) of medetomidine with intranasal drops (IND) and intramuscular (IM) injection in healthy dogs. Study designProspective, blinded, randomized study. AnimalsA group of 18 mixed-breed shelter-owned dogs weighing 27 ± 4.3 kg (mean ± standard deviation). MethodsThe dogs were randomly assigned to equal groups of six dogs for administration of medetomidine (40 μg kg−1) by INA, IND and IM routes. Ease of administration was evaluated using a resistance scale. Composite sedation score (CSS), heart rate (HR) and respiratory frequency (fR) were measured immediately before (T0, baseline) and after drug administration at time points 15, 45, 75 and 120 minutes. The time of onset of sedation was recorded. Ease of administration and onset of sedation were analysed by the Kruskal–Wallis and post hoc Dunn’s tests. Repeated measures analysis of anova and least significant difference tests were used to analyse CSS, HR and fR over time. Tukey’s post hoc test was used for time point comparisons among groups. Significance was set at p < 0.05. ResultsNo differences were detected among groups for ease of administration (p = 0.346). CSS increased in all groups from baseline values. Onset of sedation in IM was 6.3 ± 2.0 minutes, in INA was 7.2 ± 2.5 minutes and in IND was 20.7 ± 5.4 minutes. CSS in IND was lower than in the other groups at T15 and lower than in INA at T45. CSS was not different between IM and INA. HR and fR decreased in all groups compared with respective baseline values. HR in IND was lower than in IM at T45–T120. Conclusions and clinical relevanceINA medetomidine (40 μg kg−1) can be an alternative and noninvasive route to IM injections for sedating healthy dogs. IND resulted in a slow onset of sedation.