Effects of sedation on echocardiographic variables of left atrial and left ventricular function in healthy cats

Although sedation is frequently used to facilitate patient compliance in feline echocardiography, the effects of sedative drugs on echocardiographic variables have been poorly documented. This study investigated the effects of two sedation protocols on echocardiographic indices in healthy cats, with special emphasis on the assessment of left atrial size and function, as well as left ventricular diastolic performance. Seven cats underwent echocardiography (transthoracic two-dimensional, spectral Doppler, color flow Doppler and tissue Doppler imaging) before and after sedation with both acepromazine (0.1 mg/kg IM) and butorphanol (0.25 mg/kg IM), or acepromazine (0.1 mg/kg IM), butorphanol (0.25 mg/kg IM) and ketamine (1.5 mg/kg IV). Heart rate increased significantly following acepromazine/butorphanol/ketamine (mean ± SD of increase, 40 ± 26 beats/min) and non-invasive systolic blood pressure decreased significantly following acepromazine/butorphanol (mean ± SD of decrease, 12 ± 19 mmHg). The majority of echocardiographic variables were not significantly different after sedation compared with baseline values. Both sedation protocols resulted in mildly decreased left ventricular end-diastolic dimension and mildly increased left ventricular end-diastolic wall thickness. This study therefore failed to demonstrate clinically meaningful effects of these sedation protocols on echocardiographic measurements, suggesting that sedation with acepromazine, butorphanol and/or ketamine can be used to facilitate echocardiography in healthy cats.     

Evaluation of the sedative and cardiorespiratory effects of dexmedetomidine,dexmedetomidine-butorphanol,and dexmedetomidine-ketamine in cats

OBJECTIVE: To determine sedative and cardiorespiratory effects of dexmedetomidine alone and in combination with butorphanol or ketamine in cats. DESIGN: Randomized crossover study. ANIMALS: 6 healthy adult cats. PROCEDURES: Cats were given dexmedetomidine alone (10 microg/kg [4.5 mg/lb], IM), a combination of dexmedetomidine (10 microg/kg, IM) and butorphanol (0.2 mg/kg [0.09 mg/lb], IM), or a combination of dexmedetomidine (10 microg/kg, IM) and ketamine (5 mg/kg [2.3 mg/lb], IM). Treatments were administered in random order, with > or = 1 week between treatments. Physiologic variables were assessed before and after drug administration. Time to lateral recumbency, duration of lateral recumbency, time to sternal recumbency, time to recovery from sedation, and subjective evaluation of sedation, muscle relaxation, and auditory response were assessed. RESULTS: Each treatment resulted in adequate sedation; time to lateral recumbency, duration of lateral recumbency, and time to recovery from sedation were similar among treatments. Time to sternal recumbency was significantly greater after administration of dexmedetomidine-ketamine. Heart rate decreased significantly after each treatment; however, the decrease was more pronounced after administration of dexmedetomidine-butorphanol, compared with that following the other treatments. Systolic and diastolic blood pressure measurements decreased significantly from baseline with all treatments; 50 minutes after drug administration, mean blood pressure differed significantly from baseline only when cats received dexmedetomidine and butorphanol. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that in cats, administration of dexmedetomidine combined with butorphanol or ketamine resulted in more adequate sedation, without clinically important cardiovascular effects, than was achieved with dexmedetomidine alone.     

Clinical efficacy and safety of dexmedetomidine and buprenorphine, butorphanol or diazepam for canine hip radiography

OBJECTIVES: To investigate the usefulness of dexmedetomidine for restraint and sedation during hip radiographic examination of hip-extended or stress-radiography views when combined with either buprenorphine, butorphanol or diazepam. METHODS: One hundred and twenty-seven client-owned clinically healthy golden retrievers or rottweilers were enrolled in a clinical trial that compared hip-extended and PennHIP methods for diagnosing hip dysplasia and were randomly allocated to receive dexmedetomidine or medetomidine in combination with buprenorphine, butorphanol or diazepam. Subjective assessments were made for response to pain, response to noise, palpebral reflex, muscle tone and overall quality of sedation; non-invasive physiological variables were also recorded. RESULTS: Overall quality of sedation was graded as good or excellent for dogs administered with a combination of butorphanol or diazepam. However, more dogs that received a combination involving buprenorphine had overall a relatively poorer quality of sedation and required additional administration of buprenorphine before the radiographic procedure could commence. Once sedated, clinically sufficient muscle relaxation accompanied by a very low proportion of dogs responding to pain or noise stimuli were observed in all treatment groups. Heart and respiratory rate, and procedure and recovery times were similar for all treatment groups, and no adverse events were observed during the study. CLINICAL SIGNIFICANCE: Dexmedetomidine sedative protocols, particularly in combination with butorphanol and diazepam, can be used effectively and safely in dogs for radiographic procedures.     

Sedative, cardiovascular, haematologic and biochemical effects of four different drug combinations administered intramuscularly in cats

ObjectiveTo compare effects of four drug combinations on sedation, echocardiographic, haematologic and biochemical variables and recovery in cats.Study designExperimental randomized ‘blinded’ cross-over study.AnimalsSix healthy cats.Materials and MethodsTreatments were administered intramuscularly: midazolam 0.4 mg kg^?1 and butorphanol 0.4 mg kg^?1 (MB); midazolam 0.4 mg kg^?1, butorphanol 0.4 mg kg^?1 and ketamine 3 mg kg^?1 (MBK); midazolam 0.4 mg kg^?1, butorphanol 0.4 mg kg^?1 and dexmedetomidine 5 μg kg^?1 (MBD); ketamine 3 mg kg^?1 and dexmedetomidine 5 μg kg^?1(KD). Sedation was evaluated at time-points over 10 minutes post injection. Echocardiography, systolic arterial blood pressure (SAP) measurement and blood sampling were performed at baseline and from 10 minutes after treatment. Quality of recovery was scored. Data were analysed by anova for repeated measures. p < 0.05 was considered significant.ResultsThe lowest sedation score was obtained by MB, (median 10.5 [7; 20]), highest by KD (36.5 [32; 38]). Quality of recovery was best with KD (0.5 [0; 2]), and worst with MB (7.5 [4; 11]). Relative to baseline measurements, treatments decreased SAP by 17%, 25%, 13%, 5% in MB, MBK, MBD and KD, respectively. Heart rate decreased (p < 0.05) after MBD (44%) and KD (34%). All treatments decreased stroke volume by 24%, 21%, 24%, 36%, and cardiac output by 23%, 34%, 54%, 53% in MB, MBK, MBD and KD, respectively. Packed cell volume was decreased (p < 0.05) by 20%, 31%, 29% in MBK, MBD and KD, respectively. Plasma glucose was increased after MBD (31%) and KD (52%) and lactate concentration was decreased (p < 0.05) after MBK (58%), MBD (72%) and KD (65%).Conclusions and clinical relevanceThe MB combination did not produce sedation in healthy cats. Treatment MBK led to acceptable sedation and minimal cardiovascular changes. Both treatments with dexmedetomidine produced excellent sedation and recovery but induced more cardiovascular depression and haematologic changes.     

EFFECT OF SEDATION ON CONTRAST‐ENHANCED ULTRASONOGRAPHY OF THE SPLEEN IN HEALTHY DOGS

Contrast‐enhanced ultrasound of the spleen enables the dynamic assessment of the perfusion of this organ, however, both subjective and quantitative evaluation can be strongly influenced by sedative agent administration. The purpose of this prospective, experimental study was to test effects of two sedative agents on splenic perfusion during contrast‐enhanced ultrasound of the spleen in a sample of healthy dogs. Contrast‐enhanced ultrasound of the spleen was repeated in six healthy Beagles following a cross‐over study design comparing three protocols: awake, butorphanol 0.2 mg/Kg intramuscular (IM), and dexmedetomidine 500 μg/m² IM. After intravenous injection of a phospholipid stabilized sulfur hexafluoride microbubble solution (SonoVue®, Bracco Imaging, Milano, Italy), the enhancement intensity and perfusion pattern of the splenic parenchyma were assessed and perfusion parameters were calculated. Normal spleen was slightly heterogeneous in the early phase, but the parenchyma was homogeneous at a later phase. Sedation with butorphanol did not modify perfusion of the spleen. Dexmedetomidine significantly reduced splenic enhancement, providing diffuse parenchymal hypoechogenicity during the entire examination. Measured parameters were significantly modified, with increased arrival time (AT; (< 0.0001) and time to peak (TTP; P < 0.0001), and decreased peak intensity (PI; P = 0.0108), wash‐in (P = 0.0014), and area under the curve (AUC; P = 0.0421). Findings supported the use of butorphanol and contraindicated the use of dexmedetomidine as sedatives for splenic contrast ultrasound procedures in dogs. Short‐term and diffuse heterogeneity of the spleen in the early venous phase was determined to be a normal finding.     

Hemodynamic effects in dogs after intramuscular administration of a combination of dexmedetomidine-butorphanol-tiletamine-zolazepam or dexmedetomidine-butorphanol-ketamine

Objective-To evaluate hemodynamic effects in dogs after IM administration of dexmedetomidine (7.5 μg/kg, butorphanol (0.15 mg/kg), and tiletamine-zolazepam (3 mg/kg [DBTZ]) or dexmedetomidine (15 μg/kg), butorphanol (0.3 mg/kg), and ketamine (3 mg/kg [DBK]). Animals-5 healthy adult mixed-breed dogs. Procedures-Each dog received DBTZ and DBK in a randomized crossover study with a 48-hour interval between treatments. Anesthesia was induced and maintained with sevoflurane in 100% oxygen while instrumentation with Swan-Ganz and arterial catheters was performed. Following instrumentation, hemodynamic measurements were recorded at 3.54% (1.5 times the minimum alveolar concentration) sevoflurane; then sevoflurane administration was discontinued, and dogs were allowed to recover. Six hours after cessation of sevoflurane administration, baseline hemodynamic measurements were recorded, each dog was given an IM injection of DBTZ or DBK, and hemodynamic measurements were obtained at predetermined intervals for 70 minutes. Results-DBTZ and DBK induced hypoventilation (Paco(2), approx 60 to 70 mm Hg), respiratory acidosis (pH, approx 7.2), hypertension (mean arterial blood pressure, approx 115 to 174 mm Hg), increases in systemic vascular resistance, and reflex bradycardia. Cardiac output, oxygen delivery, and oxygen consumption following DBTZ or DBK administration were similar to those following sevoflurane administration to achieve a surgical plane of anesthesia. Blood l-lactate concentrations remained within the reference range at all times for all protocols. Conclusions and Clinical Relevance-In healthy dogs, both DBTZ and DBK maintained oxygen delivery and oxygen consumption to tissues and blood lactate concentrations within the reference range. However, ventilation should be carefully monitored and assisted when necessary to prevent hypoventilation.     

Sedative effects of dexmedetomidine,dexmedetomidine–pethidine and dexmedetomidine–butorphanol in cats

The purpose of this study was to assess the clinical effects of dexmedetomidine, both alone and combined with pethidine or butorphanol, in cats. A prospective randomized blind study was performed. Thirty cats were randomly assigned to three groups of 10 animals: D: dexmedetomidine (20 μg/kg IM); DP: dexmedetomidine (10 μg/kg IM) and pethidine (2.5 mg/kg IM); DB: dexmedetomidine (10 μg/kg IM) and butorphanol (0.4 mg/kg IM). Quality of sedation, analgesia, muscle relaxation and the possibility of performing some clinical procedures were compared using a multifactorial scale. Sedation, analgesia and muscle relaxation increased progressively over time and did not differ in the three protocols. The three protocols facilitated the completion of several clinical procedures. The clinical variables studied showed a similar behaviour in the three protocols and remained close to the baseline, except for a drop in heart rate in protocol D. In conclusion, dexmedetomidine, either alone or combined with pethidine or butorphanol, offers suitable sedation, analgesia and relaxation to perform various clinical procedures in cats.     

Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha2-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 microg/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha2-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the alpha2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.     

The pharmacokinetics of dexmedetomidine administered as a constant rate infusion in horses

Dexmedetomidine, the most selective α₂‐adrenoceptor agonist in clinical use, is increasingly being used in both conscious and anaesthetized horses; however, the pharmacokinetics and sedative effects of this drug administered alone as an infusion are not previously described in horses. Seven horses received an infusion of 8 μg dexmedetomidine/kg/h for 150 min, venous blood samples were collected, and dexmedetomidine concentrations were assayed using liquid chromatography‐mass spectrometry (LC/MS) and analyzed using noncompartmental pharmacokinetic analysis. Sedation was scored as the distance from the lower lip of the horse to the ground measured in centimetre. The harmonic mean (SD) plasma elimination half‐life (Lambda z half‐life) for dexmedetomidine was 20.9 (5.1) min, clearance (Cl) was 0.3 (0.20) L/min/kg, and volume of distribution at steady‐state (Vd_ss) was 13.7 (7.9) L/kg. There was a considerable individual variation in the concentration of dexmedetomidine vs. time profile. The level of sedation covaried with the plasma concentration of dexmedetomidine. This implies that for clinical use of dexmedetomidine constant rate infusion in conscious horses, infusion rates can be easily adjusted to effect, and this is preferable to an infusion at a predetermined value.     

Effects of acepromazine and dexmedetomidine,followed by propofol induction and maintenance with isoflurane anaesthesia,on the microcirculation of Beagle dogs evaluated by sidestream dark field imaging: an experimental trial

ObjectiveTo investigate the effects of intramuscularly administered acepromazine or dexmedetomidine on buccal mucosa microcirculation in Beagle dogs.Study designExperimental, blinded, crossover study.AnimalsA group of seven Beagle dogs aged 7.5 ± 1.4 years (mean ± standard deviation).MethodsMicrocirculation was assessed on buccal mucosa using sidestream dark field videomicroscopy. After baseline measurements, 5 μg kg^–1 dexmedetomidine or 30 μg kg^–1 acepromazine were administered intramuscularly. After 10, 20 and 30 minutes, measurements were repeated. At 40 minutes after premedication, anaesthesia was induced with propofol intravenously and maintained with isoflurane. Measurements were repeated 50, 60 and 65 minutes after the injection of the investigated drugs. Analysed microcirculatory variables were: Perfused de Backer density, Perfused de Backer density of vessels < 20 μm, Proportion of perfused vessels and Proportion of perfused vessels < 20 μm. Heart rate (HR), systolic, diastolic (DAP) and mean (MAP) arterial pressures were recorded at the same time points. Macro- and microcirculatory variables were analysed using a linear mixed model with baseline as a covariate, treatment, trial period and repetition as fixed effects and time and dog as random effect. Results are presented as effect size and confidence interval; p values < 0.05 were considered significant.ResultsAfter acepromazine, Perfused de Backer density was greater during sedation and anaesthesia [3.71 (1.93–5.48 mm mm^–2, p < 0.0001) and 2.3 (0.86–3.75 mm mm^–2, p < 0.003)], respectively, than after dexmedetomidine. HR was significantly lower, whereas MAP and DAP were significantly higher with dexmedetomidine during sedation and anaesthesia (p < 0.0001 for all) compared with acepromazine.Conclusions and clinical relevanceThe sedative drugs tested exerted a significant effect on buccal mucosal microcirculation with a higher Perfused de Backer density after the administration of acepromazine compared with dexmedetomidine. This should be considered when microcirculation is evaluated using these drugs.     

Combination of dexmedetomidine with buprenorphine enhances the antinociceptive effect to a thermal stimulus in the cat compared with either agent alone

ObjectiveTo evaluate the sedative and antinociceptive effects of combinations of dexmedetomidine and buprenorphine in cats.Study designExperimental randomized study.AnimalsTwelve purpose-bred neutered domestic short-hair cats (4 male and 8 female) weighing 4.6 kg (range 3.7–5.5 kg) aged from 2 to 5 years.MethodsSix cats per group were administered buprenorphine (B) at 10 (B10) or 20 μg kg^?1 (B20) or dexmedetomidine (D) at 20 (D20) or 40 μg kg^?1 (D40) or a combination of B10/D20. A feline thermal nociceptive threshold testing device was used to evaluate the antinociceptive effects of the drugs before and up to 24 hours after drug treatment. Sedation was scored using a 100 mm visual analogue scale (VAS).ResultsThermal thresholds increased significantly after administration of all but D20. Area under the curve (AUC, hours °C) for the first 6 hours (mean ± SD) for B20 (281 ± 17.8) was significantly greater than B10 (260 ± 11.4), D20 (250 ± 7.9) and D40 (255 ± 11.4). The AUC for B10/D20 (273 ± 12.2) was significantly greater than D20 but not the other treatments. No sedation was seen after administration of B10 or B20 and maximal sedation was seen for all animals in the D40 and B10/D20 groups and most animals in the D20 group.ConclusionsD20 alone had the smallest analgesic effect; B10 alone provided no sedation but their combination gave good sedation with analgesia comparable with B20.Clinical relevanceThis combination could be a useful multimodal sedative/analgesic regimen in cats.     

Sedative and analgesic effects of buprenorphine,combined with either acepromazine or dexmedetomidine,for premedication prior to elective surgery in cats and dogs

ObjectiveTo evaluate the sedative and analgesic effects of intramuscular buprenorphine with either dexmedetomidine or acepromazine, administered as premedication to cats and dogs undergoing elective surgery.Study designProspective, randomized, blinded clinical study.AnimalsForty dogs and 48 cats.MethodsAnimals were assigned to one of four groups, according to anaesthetic premedication and induction agent: buprenorphine 20 μg kg^?1 with either dexmedetomidine (dex) 250 μg m^?2 or acepromazine (acp) 0.03 mg kg^?1, followed by alfaxalone (ALF) or propofol (PRO). Meloxicam was administered preoperatively to all animals and anaesthesia was always maintained using isoflurane. Physiological measures and assessments of pain, sedation and mechanical nociceptive threshold (MNT) were made before and after premedication, intraoperatively, and for up to 24 hours after premedication. Data were analyzed with one-way, two-way and mixed between-within subjects anova, Kruskall–Wallis analyses and Chi squared tests. Results were deemed significant if p ≤ 0.05, except where multiple comparisons were performed (p ≤ 0.005).ResultsCats premedicated with dex were more sedated than cats premedicated with acp (p < 0.001) and ALF doses were lower in dex cats (1.2 ± 1.0 mg kg^?1) than acp cats (2.5 ± 1.9 mg kg^?1) (p = 0.041). There were no differences in sedation in dogs however PRO doses were lower in dex dogs (1.5 ± 0.8 mg kg^?1) compared to acp dogs (3.3 ± 1.1 mg kg^?1) (p < 0.001). There were no differences between groups with respect to pain scores or MNT for cats or dogs.ConclusionChoice of dex or acp, when given with buprenorphine, caused minor, clinically detectable, differences in various characteristics of anaesthesia, but not in the level of analgesia.Clinical relevanceA combination of buprenorphine with either acp or dex, followed by either PRO or ALF, and then isoflurane, accompanied by an NSAID, was suitable for anaesthesia in dogs and cats undergoing elective surgery. Choice of sedative agent may influence dose of anaesthetic induction agent.     

Standing sedation in captive zebra (Equus grevyi and Equus burchellii)

Nine Grevy's zebras (Equus grevyi) and three Burchell's zebras (Equus burchellii) were immobilized in a standing position a total of 70 times for minor, nonpainful procedures over a 9-yr period. Standing sedation was successfully obtained with a combination of detomidine and butorphanol on 47 occasions (67.1%). Detomidine i.m. (median 0.10 mg/kg; range: 0.07-0.21) was administered by dart, followed 10 min later by butorphanol i.m. (median 0.13 mg/kg; range 0.04-0.24). The dosages were varied depending on the initial demeanor of the animal. On 23 occasions (32.9%), small amounts of etorphine (median 2.5 microg/kg; range 1.1-12.3 microg/kg) plus acepromazine (median 10 microg/kg; range 4.4-50 microg/kg) (as in Large Animal-Immobilon) had to be administered i.m. to gain sufficient sedation. In these latter cases, the animals were either excited or known for their aggressive character. The zebras were sufficiently immobilized for the length of most procedures (<45 min) without supplementation. At the end of the procedure, the animals were given atipamezole (2 mg per 1 mg detomidine used) and naltrexone (0.1 mg/kg) to reverse the sedative effects, irrespective of whether etorphine was used or not. Standing sedation, using the combination of the alpha-2 agonist detomidine and the partial agonist-antagonist opioid butorphanol (in some cases supplemented with etorphine + acepromazine), proved to be a very efficacious and safe method to be used in zebras under zoo conditions for short-lasting, nonpainful procedures.     

Cardiopulmonary effects and recovery characteristics associated with 2 sedative protocols for assisted ventilation in healthy neonatal foals

Neonatal foals may require prolonged sedation to permit ventilatory support in the first few days of life. The objective of this study was to evaluate and compare the cardiopulmonary effects and clinical recovery characteristics of 2 sedative/analgesia protocols in healthy foals receiving assisted ventilation. Foals were randomized to receive dexmedetomidine, butorphanol, and propofol (DBP) or midazolam, butorphanol, and propofol (MBP) during a 24-hour period. Infusion rates of dexmedetomidine, midazolam, and propofol were adjusted and propofol boluses administered according to set protocols to maintain optimal sedation and muscle relaxation. Ventilatory support variables were adjusted to preset targets. Physiologic variables were recorded, cardiac output (CO) measured (thermodilution), and arterial and mixed venous blood collected for gas analysis at intervals up to 24 hours. Foals in group DBP received dexmedetomidine [2.4 ± 0.5 μg/kg body weight (BW) per hour], butorphanol (13 μg/kg BW per hour), and propofol (6.97 ± 0.86 mg/kg BW per hour), whereas foals in group MBP received midazolam (0.14 ± 0.04 mg/kg BW per hour), butorphanol (13 μg/kg BW per hour), and propofol (5.98 ± 1.33 mg/kg BW per hour). Foals in the DBP group received significantly more propofol boluses (9.0 ± 3.0) than those in the MBP group (4.0 ± 2.0). Although physiologic variables remained within acceptable limits, heart rate (HR), mean arterial pressure (MAP), and cardiac index (CI) were lower in foals in the DBP group than in the MBP group. Times to sternal recumbency, standing, and nursing were significantly shorter in the DBP than MBP group. We found that MBP and DBP protocols are suitable to assist ventilatory support in neonatal foals, although MBP results in a prolonged recovery compared to DBP.     

Effects of intramuscular sedative and opioid combinations on tear production in dogs

The effect of commonly used sedation protocols on tear production rate was evaluated in dogs. Schirmer I tear tests were examined before and after intramuscular injection of acepromazine and oxymorphone (ACE + OXY; n  = 7), diazepam and butorphanol (DIA + BUT; n  = 8), and xylazine and butorphanol (XYL + BUT; n  = 8). Two Schirmer I tear tests were also performed 15–25 min apart in dogs which received no sedative drugs (control; n  = 4). Tear production rate decreased to 15 ± 2, 17 ± 1, and 6 ± 1 mm min⁻¹, respectively, while control animals averaged 21 ± 2 mm min⁻¹ at the same time point. Because XYL + BUT profoundly decreased tear production rate, we evaluated the two drugs separately. While BUT mildly decreased tear production when given alone to dogs (18 ± 1 mm min⁻¹; n  = 5), xylazine had no effect on tear production. Thus it appears that the two agents act synergistically to decrease tear production rate in dogs. Moreover, sterile ocular lubricant or tear replacement should be used during XYL + BUT sedation.     

Plasma concentrations and sedative effects of a dexmedetomidine,midazolam, and butorphanol combination after transnasal administration in healthy rabbits

Plasma concentrations of dexmedetomidine (D = 0.1 mg/kg), midazolam (M = 2 mg/kg), and butorphanol (B = 0.4 mg/kg) were analyzed by liquid chromatography–mass spectrometry (LC–MS/MS) after their simultaneous (DMB) transnasal (TN) administration to healthy rabbits. Time‐dependent changes in sedation and antinociception were evaluated by measuring a sedation score based on rabbit's posture, loss of the righting, palpebral and pedal withdrawal reflexes and by instrumental monitoring of rectal temperature, heart rate, arterial blood pressure, pulse‐oximetry, and capnometry. The peak plasma concentration (C_max) of each drug was reached within 5 min (T_max) from DMB‐TN administration along with deep sedation and analgesia. Such effects subsided after 45 min into a moderate sedation and analgesia lasting for additional 15 min. All rabbits awakened spontaneously and uneventfully 90 min after DMB‐TN administration. During the anesthetic procedure, arterial blood pressure markedly decreased and respiratory depression ensued requiring oxygen supplementation. The results of this study show that all three molecules of the DMB combination were absorbed through the TN route, inducing deep sedation and analgesia suitable for minor surgical procedures. Such combination should be used with caution in rabbits bearing cardiovascular or respiratory diseases because of its ability to induce hypotension and respiratory depression.     

Two doses of dexmedetomidine in combination with buprenorphine for premedication in dogs; a comparison with acepromazine and buprenorphine

ObjectiveTo assess as premedicants, the sedative, cardiorespiratory and propofol-sparing effects in dogs of dexmedetomidine and buprenorphine compared to acepromazine and buprenorphine.Study designProspective, randomised, blinded clinical studyAnimalsSixty healthy dogs (ASA grades I/II). Mean (SD) body mass 28.0 ± 9.1 kg, and mean age 3.4 ± 2.3 years.MethodsDogs were allocated randomly to receive 15 μg kg^?1 buprenorphine combined with either 30 μg kg^?1 acepromazine (group 1), 62.5 μg m^?2 dexmedetomidine (group 2), or 125 μg m^?2 dexmedetomidine (group 3) intramuscularly. After 30 minutes, anaesthesia was induced using a propofol target controlled infusion. Heart rate, respiratory rate, and oscillometric arterial blood pressure were recorded prior to induction, at endotracheal intubation and at 3 and 5 minutes post-intubation. Induction quality and pre-induction sedation were scored on 4 point scales. Propofol target required for endotracheal intubation was recorded. Data were analysed using Chi-squared tests, Kruskal-Wallis, one way and general linear model anova (p < 0.05).ResultsAge was significantly lower in group 1 (1.0 (1.0–3.8) years) than group 2 (5.0 (2.0–7.0) years), (median, (IQR)). There were no significant differences in sedation or quality of induction between groups. After premedication, heart rate was significantly lower and arterial blood pressures higher in groups 2 and 3 than group 1, but there was no significant difference between groups 2 and 3. Propofol targets were significantly lower in group 3 (1.5 (1.0–2.5) μg mL^?1) than group 1 (2.5 (2.0–3.0) μg mL^?1); no significant differences existed between group 2 (2.0 (1.5–2.5) μg mL^?1) and the other groups (median, (interquartile range)).Conclusions and Clinical relevanceWhen administered with buprenorphine, at these doses, dexmedetomidine had no advantages in terms of sedation and induction quality over acepromazine. Both doses of dexmedetomidine produced characteristic cardiovascular and respiratory effects of a similar magnitude.