Effects of tasipimidine premedication with and without methadone and dexmedetomidine on cardiovascular variables during propofol-isoflurane anaesthesia in Beagle dogs.

OBJECTIVE: To evaluate cardiovascular effects of oral tasipimidine on propofol-isoflurane anaesthesia with or without methadone and dexmedetomidine at equianaesthetic levels. STUDY DESIGN: Prospective, placebo-controlled, blinded, experimental trial. ANIMALS: A group of seven adult Beagle dogs weighing (mean ± standard deviation) 12.4 ± 2.6 kg and a mean age of 20.6 ± 1 months. METHODS: The dogs underwent four treatments 60 minutes before induction of anaesthesia with propofol. PP: placebo orally and placebo (NaCl 0.9%) intravenously (IV); TP: tasipimidine 30 µg kg-1 orally and placebo IV; TMP: tasipimidine 30 µg kg-1 orally and methadone 0.2 mg kg-1 IV; and TMPD: tasipimidine 30 µg kg-1 orally with methadone 0.2 mg kg-1 and dexmedetomidine 1 µg kg-1 IV followed by 1 µg kg-1 hour-1. Isoflurane in oxygen was maintained for 120 minutes at 1.2 individual minimum alveolar concentration preventing motor movement. Cardiac output (CO), tissue blood flow (tbf), tissue oxygen saturation (stO2) and relative haemoglobin content were determined. Arterial and mixed venous blood gases, arterial and pulmonary artery pressures and heart rate (HR) were measured at baseline; 60 minutes after oral premedication; 5 minutes after IV premedication; 15, 30, 60, 90 and 120 minutes after propofol injection; and 30 minutes after switching the vaporiser off. Data were analysed by two-way anova for repeated measures; p < 0.05. RESULTS: Tasipimidine induced a significant 20-30% reduction in HR and CO with decreases in MAP (10-15%), tbf (40%) and stO2 (43%). Blood pressure and oxygenation variables were mainly influenced by propofol-isoflurane-oxygen anaesthesia, preceded by short-lived alterations related to IV methadone and dexmedetomidine. CONCLUSIONS AND CLINICAL RELEVANCE: Tasipimidine induced mild to moderate cardiovascular depression. It can be incorporated into a common anaesthetic protocol without detrimental effects in healthy dogs, when anaesthetics are administered to effect and cardiorespiratory function is monitored.

Ketamine-propofol for total intravenous anaesthesia in rabbits: a comparison of premedication with acepromazine-medetomidine, acepromazine-midazolam or acepromazine-morphine.

OBJECTIVE: To describe ketamine-propofol total intravenous anaesthesia (TIVA) following premedication with acepromazine and either medetomidine, midazolam or morphine in rabbits. STUDY DESIGN: Randomized, crossover experimental study. ANIMALS: A total of six healthy female New Zealand White rabbits (2.2 ± 0.3 kg). METHODS: Rabbits were anaesthetized on four occasions, each separated by 7 days: an intramuscular injection of saline alone (treatment Saline) or acepromazine (0.5 mg kg-1) in combination with medetomidine (0.1 mg kg-1), midazolam (1 mg kg-1) or morphine (1 mg kg-1), treatments AME, AMI or AMO, respectively, in random order. Anaesthesia was induced and maintained with a mixture containing ketamine (5 mg mL-1) and propofol (5 mg mL-1) (ketofol). Each trachea was intubated and the rabbit administered oxygen during spontaneous ventilation. Ketofol infusion rate was initially 0.4 mg kg-1 minute-1 (0.2 mg kg-1 minute-1 of each drug) and was adjusted to maintain adequate anaesthetic depth based on clinical assessment. Ketofol dose and physiological variables were recorded every 5 minutes. Quality of sedation, intubation and recovery times were recorded. RESULTS: Ketofol induction doses decreased significantly in treatments AME (7.9 ± 2.3) and AMI (8.9 ± 4.0) compared with treatment Saline (16.8 ± 3.2 mg kg-1) (p < 0.05). The total ketofol dose to maintain anaesthesia was significantly lower in treatments AME, AMI and AMO (0.6 ± 0.1, 0.6 ± 0.2 and 0.6 ± 0.1 mg kg-1 minute-1, respectively) than in treatment Saline (1.2 ± 0.2 mg kg-1 minute-1) (p < 0.05). Cardiovascular variables remained at clinically acceptable values, but all treatments caused some degree of hypoventilation. CONCLUSIONS AND CLINICAL RELEVANCE: Premedication with AME, AMI and AMO, at the doses studied, significantly decreased the maintenance dose of ketofol infusion in rabbits. Ketofol was determined to be a clinically acceptable combination for TIVA in premedicated rabbits.

Sedative effects and changes in cardiac rhythm with intravenous premedication of medetomidine, butorphanol and ketamine in dogs.

OBJECTIVE: To determine the sedative effects and characteristics of cardiac rhythm with intravenous (IV) premedication of medetomidine, butorphanol and ketamine in dogs. STUDY DESIGN: Prospective, blinded, randomized clinical trial. ANIMALS: A total of 116 client-owned healthy dogs undergoing elective surgery. METHODS: Dogs were randomly allocated one of four groups: group M, medetomidine 5 µg kg-1; group B, butorphanol 0.2 mg kg-1; group MB, medetomidine 5 µg kg-1 and butorphanol 0.2 mg kg-1; or group MBK, medetomidine 5 µg kg-1, butorphanol 0.2 mg kg-1 and ketamine 1 mg kg-1 IV. Sedation was assessed using a numerical descriptive scale. Heart rate (HR) and rhythm were monitored; propofol dose (mg kg-1 IV) to allow orotracheal intubation was documented. Data were analysed using anova, accounting for multiple testing with the Tukey honest significant difference test. RESULTS: Sedation scores varied significantly between all groups at all time points, except between groups MB and MBK at four time points. HR decreased in all groups: most in groups M and MB, least in group B. HR was initially higher in group MBK than in groups M and MB. Arrhythmias occurred in all groups: group B showed second-degree atrioventricular blocks occasionally, all other groups showed additionally ventricular escape complexes and bundle branch blocks. Dose of propofol required for orotracheal intubation was significantly higher in group B (5.0 ± 2.0 mg kg-1) than in group M (2.6 ± 0.6 mg kg-1). Although no difference could be demonstrated between groups MB (1.4 ± 0.6 mg kg-1) and MBK (0.9 ± 0.8 mg kg-1), both groups required significantly less propofol than group M. CONCLUSION AND CLINICAL RELEVANCE: Medetomidine-based premedication protocols led to various bradyarrhythmias. Addition of subanaesthetic doses of ketamine to medetomidine-based protocols resulted in higher HRs, fewer bradyarrhythmias and fewer animals that required propofol for intubation without causing side effects in healthy dogs.

COMPARISON OF KETAMINE-MIDAZOLAM AND KETAMINE-MIDAZOLAM-BUTORPHANOL PREMEDICATION PRIOR TO SEVOFLURANE ANESTHESIA IN WOODCHUCKS (MARMOTA MONAX).

Cardiovascular disease is a frequent cause of death in the critically endangered Vancouver Island marmots (Marmota vancouverensis). This warrants the use of anesthetic protocols with minimal cardiovascular adverse effects. In this study, 12 adult male woodchucks (Marmota monax) were used as models for Vancouver Island marmots. The objective was to compare the physiological effects of two premedication protocols during induction and maintenance of anesthesia with sevoflurane. The two premedications were ketamine 10 mg/kg and midazolam 0.5 mg/kg (KM) or ketamine 10 mg/kg, midazolam 0.5 mg/kg, and butorphanol 1.0 mg/kg (KMB), administered intramuscularly prior to mask induction. Each marmot underwent three anesthetic events and protocols were assigned using a blinded randomized crossover design. Heart rate, respiratory rate, oxygen saturation, and body temperature were recorded throughout, and blood gases were assessed following induction. Resistance to induction was scored and time to induction was recorded. Although mask induction with sevoflurane was successful in all events (mean induction time of 2.1 min), KMB premedication resulted in a faster induction (mean induction time reduced by 1.2 ± 0.3 min) and lower resistance scores. Both protocols resulted in significant cardiovascular and respiratory depression; however, animals that received KMB were more hypercapnic than KM by 8.8 ± 2.8 mm Hg (P = 0.03) (mean venous partial pressure of carbon dioxide [PvCO2] for all: 79.9 mm Hg). In conclusion, if shorter induction times are desired, KMB premedication is preferred. However, cardiorespiratory variables including blood pressure should be monitored, and endotracheal intubation is recommended to allow for ETCO2 monitoring and provision of intermittent positive pressure ventilation.

Comparison between dexmedetomidine and acepromazine in combination with methadone for premedication in brachycephalic dogs undergoing surgery for brachycephalic obstructive airway syndrome.

OBJECTIVE: To compare dexmedetomidine with acepromazine for premedication combined with methadone in dogs undergoing brachycephalic obstructive airway syndrome (BOAS) surgery. STUDY DESIGN: Randomized, blinded clinical study. ANIMALS: A group of 40 dogs weighing mean (± standard deviation) 10.5 ± 6 kg, aged 2.6 ± 1.9 years. METHODS: Dogs received either acepromazine 20 µg kg-1 (group A) or dexmedetomidine 2 µg kg-1 (group D) intramuscularly with methadone 0.3 mg kg-1. Anaesthesia was induced with propofol and maintained with sevoflurane. Sedation (0-18), induction (0-6) and recovery (0-5) qualities were scored. Propofol dose, hypotension incidence, mechanical ventilation requirement, extubation time, additional sedation, oxygen supplementation, regurgitation and emergency intubation following premedication or during recovery were recorded. Data were analysed using t tests, Mann-Whitney U or Chi-square tests. RESULTS: Group A dogs were less sedated [median (range): 1.5 (0-12)] than group D [5 (1-18)] (p = 0.021) and required more propofol [3.5 (1-7) versus 2.4 (1-8) mg kg-1; p = 0.018]. Induction scores [group A: 5 (4-5); group D 5 (3-5)] (p = 0.989), recovery scores [group A 5 (4-5); group D 5(3-5)](p = 0.738) and anaesthesia duration [group A:93 (50-170); group D 96 (54-263) minutes] (p = 0.758) were similar between groups. Time to extubation was longer in group A 12.5 (3-35) versus group D 5.5 (0-15) minutes; (p = 0.005). During recovery, two dogs required emergency intubation (p > 0.99) and five dogs required additional sedation (p > 0.99). Oxygen supplementation was required in 16 and 12 dogs in group A and D, respectively (p = 0.167); no dogs in group A and one dog in group D regurgitated (p = 0.311). CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine 2 µg kg-1 produces more sedation but similar recovery quality to acepromazine 20 µg kg-1 combined with methadone in dogs undergoing BOAS surgery.

Comparison of the effects of methadone and butorphanol combined with acepromazine for canine gastroduodenoscopy.

OBJECTIVE: To evaluate the feasibility of gastroduodenoscopy in dogs premedicated with acepromazine in combination with butorphanol or methadone. STUDY DESIGN: Prospective, randomized, double-blinded clinical trial. ANIMALS: A group of 40 client-owned dogs. METHODS: Dogs were randomly allocated to one of two groups and give intramuscular acepromazine 0.02 mg kg-1 combined with either butorphanol 0.3 mg kg-1 (group ACEBUT) or methadone 0.2 mg kg-1 (group ACEMET). General anaesthesia was induced with propofol and ketamine and maintained with sevoflurane (2.3%) in oxygen. Cardiopulmonary variables were recorded at 5 minute intervals during anaesthesia. Feasibility of the entire gastroduodenoscopy was evaluated with a visual analogue scale (VAS) from 0 (best) to 100 (worst) (primary outcome of the study). Lower oesophageal sphincter dilatation and duodenal intubation were scored. Pylorus diameter was measured with standard endoscopic inflatable balloons. Overall cardiovascular stability was assessed during anaesthesia, using a VAS (0-100), as was the presence of fluid in the oesophagus, regurgitation, need for mechanical ventilation, and intraoperative and postoperative rescue analgesia (secondary outcomes of the study). Differences between treatments were analysed with Mann-Whitney U, Student t test, Fisher exact test or mixed model analysis of variance as appropriate. Subsequently, feasibility VAS of the gastroduodenoscopy was assessed for noninferiority between groups. The noninferiority margin was set as -10. RESULTS: All gastroduodenoscopies were successfully completed in both groups using an endoscope tip diameter of 12.8 mm in all but one dog. Feasibility of gastroduodenoscopy was evaluated as 2.9 ± 5.6 in group ACEBUT and 5.1 ± 5.8 in group ACEMET. No significant differences between groups were detected in any measured or assessed variables, and noninferiority was confirmed. CONCLUSION AND CLINICAL RELEVANCE: In our study population, the effects of methadone and butorphanol when combined with acepromazine were comparable.

ORAL HALOPERIDOL PREMEDICATION TO REDUCE CAPTURE STRESS PRIOR TO XYLAZINE-KETAMINE ANESTHESIA IN CAPTIVE SPOTTED DEER (AXIS AXIS).

A prospective clinical trial was performed to evaluate the efficacy of haloperidol premedication prior to xylazine-ketamine anesthesia with a goal of reducing capture stress in adult male captive spotted deer (Axis axis). On the morning of the study, deer were fed a banana either containing haloperidol tablets (1 mg/kg) (haloperidol group, n = 10) or without haloperidol (placebo group, n = 10). Six hours postadministration, xylazine (3 mg/kg) and ketamine (2 mg/kg) was administered intramuscularly via a dart. Rectal temperature, heart rate, respiratory rate, and SpO2 (percent hemoglobin saturation) were recorded at 5-min intervals. Blood gas analysis was performed at time 0 (venous blood) and 10 and 20 min (arterial blood) postinduction. Serum cortisol was determined from venous blood (35 min postinduction), following which yohimbine was administered at a dose of 0.15 mg/kg intramuscular and 0.15 mg/kg intravenous. Statistical analysis of repeated measures data was performed with a two-way analysis of variance. Paired data were analyzed with a Wilcoxon rank-sum test (categorical data) or a paired t-test (continuous data). Significance was set at P ≤ 0.05, and results were expressed as mean ± SEM. There was no significant difference in induction time or recovery time between treatment groups. Rectal temperature and heart rate were significantly lower in the haloperidol group. Both groups demonstrated acidosis with venous pH being significantly lower in the placebo group when compared to the haloperidol group. Serum cortisol and arterial plasma lactate were lower in the haloperidol group indicative of reduced stress and physical exertion. Haloperidol premedication proved to be beneficial in reducing capture stress, when administered prior to xylazine-ketamine anesthesia, in spotted deer.

Use of midazolam in combination with medetomidine for premedication in healthy dogs.

OBJECTIVE: To assess the sedative effects, propofol sparing properties and impact on quality of induction and intubation of intravenous (IV) medetomidine and midazolam administered consecutively at different doses compared to medetomidine alone in healthy dogs for premedication. STUDY DESIGN: Prospective, randomized, blinded, clinical study. ANIMALS: A total of 40 adult healthy client owned dogs, weighing 18 ± 7 kg (mean ± standard deviation). METHODS: Dogs were assigned to four groups: medetomidine 15 µg kg-1 (positive control group), medetomidine 10 µg kg-1 and midazolam 0.2 mg kg-1, medetomidine 5 µg kg-1 and midazolam 0.3 mg kg-1, and medetomidine 5 µg kg-1 and midazolam 0.2 µg kg-1. The same clinician assessed sedation after administration at T2.5 minutes and T5 minutes using a composite simple descriptive sedation scale ranging between 0 and 15 (0 = no sedation; 15 = profound sedation). The dose of propofol for induction, quality of induction, ease of intubation and any adverse events were recorded. RESULTS: There was no significant difference in sedation scores between treatment groups at T2.5 minutes or T5 minutes (p = 0.82 and p = 0.63, respectively). Administration of midazolam in combination with medetomidine resulted in 71% of dogs displaying paradoxical behaviours (p < 0.0001) such as agitation, excitation, restlessness, aggression and vocalization, which was different from pre-sedation. Propofol requirement was not different between groups. Induction and tracheal intubation quality was smooth in all groups. CONCLUSION: In healthy dogs, at the doses studied, the combination of medetomidine-midazolam administered IV for premedication provided moderate sedation but was associated with a high incidence of paradoxical behaviours. This drug combination IV is not recommended for premedication in healthy dogs.

Effect of propofol and ketamine-diazepam on intraocular pressure in healthy premedicated dogs.

OBJECTIVE: To compare the effect of propofol and ketamine/diazepam for induction following premedication on intraocular pressure (IOP) in healthy dogs. STUDY DESIGN: Prospective, quasi-experimental, unmasked, longitudinal. ANIMALS: A total of 61 client-owned dogs. METHODS: Dogs were anesthetized twice with a 4 week washout period. Premedication with dexmedetomidine (5 µg kg-1) and hydromorphone (0.1 mg kg-1) intramuscularly was followed by either propofol (4 mg kg-1) or ketamine (5 mg kg-1) and diazepam (0.25 mg kg-1) intravenously for induction and inhaled isoflurane for maintenance. IOP was measured by applanation tonometry using TonoPen-XL before premedication and after 5, 10, 20 and 30 minutes. IOP was measured again immediately after induction and after 3, 5, 10, 15, 20, 30 and 40 minutes. Data were analyzed using one- or two-way repeated measures ANOVA. RESULTS: No difference was found between right and left IOP (p = 0.45), and data from both the eyes of each dog were averaged and considered as one set of data. Following premedication, IOP was significantly lower at all time points than at baseline when animals were grouped together, mean difference -1.6 ± 0.2 mmHg (p < 0.05). IOP increased immediately (12.2 ± 2.4 mmHg before versus 17.1 ± 3.8 mmHg after) and at 3, 5 (p < 0.001), 10 and 40 minutes (p = 0.009 and 0.045, respectively) after propofol administration. For ketamine/diazepam, IOP was increased immediately post-induction (13.0 ± 2.7 mmHg before versus 14.7 ± 2.8 mmHg after) and at 3, 5 (p < 0.001), 30 and 40 minutes (p = 0.010 and 0.037, respectively). CONCLUSIONS AND CLINICAL RELEVANCE: Sedation with hydromorphone and dexmedetomidine significantly decreased IOP in normal dogs and may be an appropriate choice for dogs that cannot tolerate acute increases in IOP. However, IOP increased significantly after both induction protocols, abolishing the effect of premedication.

Cardiac troponin I in dogs anaesthetized with propofol and sevoflurane: the influence of medetomidine premedication and inspired oxygen fraction.

OBJECTIVE: To investigate changes in serum cardiac troponin I (cTnI) concentrations in dogs in which medetomidine was used for sedation or for premedication prior to anaesthesia with propofol and sevoflurane. STUDY DESIGN: Prospective clinical study. ANIMALS: A total of 66 client-owned dogs. METHODS: The dogs were sedated with medetomidine (0.04 mg kg-1) intravenously (IV) (group M; n = 20) and left to breath room air or anaesthetized with propofol (6.5 ± 0.76 mg kg-1 IV) and sevoflurane (4.5% vaporizer setting) in oxygen (group P + S; n = 20) or with medetomidine (0.04 mg kg-1 IV), propofol (1.92 ± 0.63 mg kg-1) and sevoflurane (3% vaporizer setting) in oxygen (group M + P + S; n = 26), respectively. After 35 minutes, medetomidine was antagonized with atipamezole (0.1 mg kg-1 intramuscularly). Blood samples for serum cTnI determination were taken before sedation or anaesthesia, 6 and 12 hours and 4 days thereafter. Serum cTnI concentrations were measured with the Architect STAT Troponin-I assay. RESULTS: Before sedation or anaesthesia, cTnI concentrations were above the detection limit in 22 out of 66 (33%) of dogs. Compared to basal values, cTnI concentrations significantly increased at 6 and 12 hours in all groups and at day 4 in group M. There were no differences in cTnI concentration between groups at baseline, at 6 hours and at 4 days. At 12 hours, cTnI concentrations were significantly higher in groups M and P + S, respectively, compared to group M + P + S. CONCLUSIONS AND CLINICAL RELEVANCE: Oxygenation during anaesthesia and reduction of propofol and sevoflurane dose due to the sparing effects of medetomidine might have played a role in alleviation of myocardial hypoxic injury as indicated by the less severe and short-lived increase of cTnI in the M + P + S group.

Effect of metoclopramide on nausea and emesis in dogs premedicated with morphine and dexmedetomidine.

OBJECTIVE: To evaluate whether subcutaneous (SC) metoclopramide (0.2 mg kg-1) administered 30 minutes prior to (T30) or simultaneously with (T0) intramuscular (IM) morphine (0.2 mg kg-1) and dexmedetomidine (0.003 mg kg-1) reduces the incidence of nausea and emesis in healthy dogs. STUDY DESIGN: Prospective, randomized and blinded study. ANIMALS: A total of 45 dogs scheduled for elective procedures. METHODS: Dogs were assigned randomly to three groups to be administered SC metoclopramide (0.2 mg kg-1) 30 minutes before (group M30) or simultaneously (group M0) to IM morphine (0.2 mg kg-1) and dexmedetomidine (0.003 mg kg-1). Dogs in the control group (group C) were administered SC saline at T30 and T0. Dogs were observed for 30 minutes after premedication to evaluate signs of nausea (continuous lip-licking and sialorrhoea) and emesis. Signs of pain or discomfort caused by SC injections were also recorded. RESULTS: There were no statistical differences amongst groups for age, body weight and sex. More dogs developed continuous lip-licking in group C (12/15, 80.0%) compared to dogs in group M30 (1/15, 6.7%) and dogs in group M0 (5/15, 33.3%; p = 0.0001 and p = 0.01, respectively). More dogs developed sialorrhoea in group M0 (8/15, 53.3%) and in group C (10/15, 66.7%) compared to dogs in group M30 (2/15, 13.3%; p = 0.03 and p = 0.004, respectively). More dogs vomited in group M0 (4/15, 26.7%) and in group C (9/15, 60.0%) compared to dogs in group M30 (0/15, 0.0%; p = 0.05 and p = 0.0003, respectively). None of the dogs demonstrated signs of pain or discomfort during SC metoclopramide injection. CONCLUSIONS AND CLINICAL RELEVANCE: Subcutaneous metoclopramide at 0.2 mg kg-1 may reduce IM morphine and dexmedetomidine-induced nausea and emesis if administered 30 minutes in advance. It is effective in reducing lip-licking even when administered concurrently with IM morphine-dexmedetomidine.

The use of alfaxalone for premedication, induction and maintenance of anaesthesia in pigs: a pilot study.

OBJECTIVE: The evaluation of alfaxalone as a premedication agent and intravenous anaesthetic in pigs. STUDY DESIGN: Prospective, clinical trial. ANIMALS: Nine healthy, 6-8-week-old female Landrace pigs weighing 22.2 ± 1.0 kg, undergoing epidural catheter placement. METHODS: All pigs were premedicated with 4 mg kg-1 alfaxalone, 40 µg kg-1 medetomidine and 0.4 mg kg-1 butorphanol administered in the cervical musculature. Sedation was subjectively scored by the same observer from 1 (no sedation) to 10 (profound sedation) prior to induction of anaesthesia with alfaxalone intravenously to effect. All pigs were maintained on alfaxalone infusions with the rate of administration adjusted to maintain appropriate anaesthetic depth. Quality of induction was scored from 1 (poor) to 3 (smooth) and basic cardiorespiratory variables were recorded every 5 minutes during anaesthesia. Results are reported as mean ± standard deviation or median (range) as appropriate. RESULTS: Sedation scores were 9 (7-10). Inductions were smooth in all pigs and cardiovascular variables remained within normal limits for the duration of anaesthesia. The induction dose of alfaxalone was 0.9 (0.0-2.3) mg kg-1. Three pigs did not require additional alfaxalone after premedication to facilitate intubation. CONCLUSIONS AND CLINICAL RELEVANCE: Intramuscular alfaxalone in combination with medetomidine and butorphanol produced moderate to deep sedation in pigs. Alfaxalone produced satisfactory induction and maintenance of anaesthesia with minimal cardiovascular side effects. Appropriate monitoring of pigs premedicated with this protocol is required as some pigs may become anaesthetized after intramuscular administration of this combination of drugs.

Do heat and moisture exchangers in the anaesthesia breathing circuit preserve body temperature in dogs undergoing anaesthesia for magnetic resonance imaging?

OBJECTIVE: To investigate whether the use of a heat and moisture exchanger (HME) preserves body temperature in dogs weighing <10 kg anaesthetised for magnetic resonance imaging (MRI). STUDY DESIGN: Prospective, randomised, clinical trial. ANIMALS: Thirty-one client-owned dogs. METHODS: Dogs were assigned randomly to a treatment group [HME (n = 16) or no HME (n = 15)]. Dogs were pseudorandomised according to the premedication they were administered, either dexmedetomidine or no dexmedetomidine. Induction agents were not standardised. General anaesthesia was maintained with isoflurane vaporised in 100% oxygen delivered using a T-piece and a fresh gas flow of 600 mL kg-1 minute-1. Rectal temperature was measured before premedication (T1), after induction (T2), before moving to the MRI unit (T3) and at the end of the MRI scan (T4). Ambient temperatures were measured in the induction room, outside and inside the MRI unit. Data were analysed using a general linear model with T4 as the outcome variable. Linear correlations were performed between T1, T2, T3 and T4, and variables that predicted T4 were investigated. RESULTS: Sex, age and body mass were not significantly different between groups. There were no significant differences in rectal temperature between groups at any time point (group with HME at the end of MRI = 36.3 ± 1.1 °C; group with no HME at the end of MRI = 36.2 ± 1.4 °C) but at the end of the MRI, dogs administered dexmedetomidine (36.6 ± 0.7 °C) had a higher rectal temperature compared with dogs not administered dexmedetomidine (35.9 ± 1.6 °C) for premedication. Rectal temperature varied directly with ambient temperature in MRI scanning room and inversely with anaesthetic duration. CONCLUSIONS AND CLINICAL RELEVANCE: Using an HME did not alter body temperature in dogs weighing <10 kg undergoing an MRI, but including dexmedetomidine in the premedication regimen seemed to preserve the body temperature during anaesthesia.

Effects of intramuscular dexmedetomidine in combination with ketamine or alfaxalone in swine.

OBJECTIVE: To evaluate and compare the use of intramuscular (IM) premedication with dexmedetomidine in combination with ketamine or alfaxalone in pigs. STUDY DESIGN: Prospective, randomized, 'blinded' trial. ANIMALS: Fourteen healthy 2-month-old Landrace × Large White pigs weighing 21.5 ± 0.6 kg. METHODS: Animals were distributed randomly into two groups: group KD (n = 7) was given 10 mg kg(-1) IM ketamine + 10 µg kg(-1) IM dexmedetomidine; and group AD (n = 7) was given 5 mg kg(-1) IM alfaxalone + 10 µg kg(-1) IM dexmedetomidine mixed in the same syringe. Pain on injection, degree of sedation and quality of induction were scored. The time from induction of anaesthesia to recumbency was recorded. Once pigs were recumbent, reflexes were evaluated. Pulse and respiratory rates, end-tidal carbon dioxide and arterial oxygen saturation were recorded at 5 and 10 minutes after drug administration. Data were compared using a two-way anova or a t-test for unpaired data as relevant. Data are presented as the mean ± standard deviation (range). RESULTS: Two animals in both groups showed slight pain on drug injection. The time to lateral recumbency in group KD [187 ± 34 seconds (153-230)] was similar to group AD [206 ± 36 seconds (150-248)]. In group AD, sedation was deeper, and the quality of anaesthetic induction was smoother. When moved for anaesthesia, five pigs in group KD vocalized. There were no differences between groups in pulse rates, arterial oxygen saturation and end-tidal carbon dioxide; however, the respiratory rate at 10 minutes was significantly higher in group KD than in group AD. CONCLUSIONS AND CLINICAL RELEVANCE: IM dexmedetomidine in combination with ketamine in pigs induced moderate to deep sedation and fair to smooth induction of anaesthesia. When dexmedetomidine was combined with alfaxalone, sedation was deeper, and induction was of a better quality.

Effects of acepromazine-morphine and acepromazine-methadone premedication on the minimum alveolar concentration of isoflurane in dogs.

OBJECTIVE: To evaluate the effects of premedication with acepromazine-morphine or acepromazine-methadone on the minimum alveolar concentration of isoflurane (ISOMAC) and the incidence of bradycardia and hypotension in dogs. STUDY DESIGN: Prospective randomized clinical study. ANIMALS: Thirty-two female dogs undergoing elective ovariohysterectomy. METHODS: Dogs were randomly assigned to one of three groups: no premedication (CONTROL group; n = 9); acepromazine (0.02 mg kg(-1)) and morphine (0.5 mg kg(-1)) (ACPMOR group; n = 11); and acepromazine (0.02 mg kg(-1)) and methadone (0.5 mg kg(-1)) (ACPMET group; n = 12). All drugs were administered intramuscularly. Twenty minutes later, anesthesia was induced with propofol administered intravenously to effect. Determinations of the ISOMAC were conducted by use of the up-and-down method using a quantal study design to determine the MAC for the population. Cardiovascular variables were registered immediately before noxious stimulation that was performed approximately 30 minutes after anesthetic induction. The occurrence of bradycardia (heart rates ≤ 70 beats minute(-1) in dogs ≤15 kg and ≤60 beats minute(-1) in dogs >15 kg) and hypotension (mean arterial pressure < 60 mmHg) were registered. RESULTS: The ISOMAC in CONTROL was 1.20 ± 0.11%. Compared with CONTROL, the ISOMAC was reduced by 33.3% and 68.3% in ACPMOR and ACPMET, respectively (p < 0.001). The ISOMAC was lower in ACPMET than in ACPMOR (p < 0.001). Bradycardia was observed in 0%, 45% and 50% of dogs and hypotension was observed in 56%, 55% and 67% of dogs in CONTROL, ACPMOR and ACPMET, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: The percentage reduction of the ISOMAC in ACPMET was approximately twice that in ACPMOR. Premedication with acepromazine-morphine or acepromazine-methadone increased the incidence of bradycardia. Hypotension was observed in most dogs during isoflurane anesthesia regardless of premedication.

Detomidine and the combination of detomidine and MK-467, a peripheral alpha-2 adrenoceptor antagonist, as premedication in horses anaesthetized with isoflurane.

OBJECTIVE: To investigate MK-467 as part of premedication in horses anaesthetized with isoflurane. STUDY DESIGN: Experimental, crossover study with a 14 day wash-out period. ANIMALS: Seven healthy horses. METHODS: The horses received either detomidine (20 µg kg(-1) IV) and butorphanol (20 µg kg(-1) IV) alone (DET) or with MK-467 (200 µg kg(-1) IV; DET + MK) as premedication. Anaesthesia was induced with ketamine (2.2 mg kg(-1) ) and midazolam (0.06 mg kg(-1) ) IV and maintained with isoflurane. Heart rate (HR), mean arterial pressure (MAP), end-tidal isoflurane concentration, end-tidal carbon dioxide tension, central venous pressure, fraction of inspired oxygen (FiO2 ) and cardiac output were recorded. Blood samples were taken for blood gas analysis and to determine plasma drug concentrations. The cardiac index (CI), systemic vascular resistance (SVR), ratio of arterial oxygen tension to inspired oxygen (Pa O2 /FiO2 ) and tissue oxygen delivery (DO2 ) were calculated. Repeated measures anova was applied for HR, CI, MAP, SVR, lactate and blood gas variables. The Student's t-test was used for pairwise comparisons of drug concentrations, induction times and the amount of dobutamine administered. Significance was set at p < 0.05. RESULTS: The induction time was shorter, reduction in MAP was detected, more dobutamine was given and HR and CI were higher after DET+MK, while SVR was higher with DET. Arterial oxygen tension and Pa O2 /FiO2 (40 minutes after induction), DO2 and venous partial pressure of oxygen (40 and 60 minutes after induction) were higher with DET+MK. Plasma detomidine concentrations were reduced in the group receiving MK-467. After DET+MK, the area under the plasma concentration time curve of butorphanol was smaller. CONCLUSIONS AND CLINICAL RELEVANCE: MK-467 enhances cardiac function and tissue oxygen delivery in horses sedated with detomidine before isoflurane anaesthesia. This finding could improve patient safety in the perioperative period. The dosage of MK-467 needs to be investigated to minimise the effect of MK-467 on MAP.

The cardiovascular effects of sevoflurane and isoflurane after premedication of healthy dogs undergoing elective surgery.

Sevoflurane and isoflurane are commonly used in veterinary anesthesia. The objective of this prospective, randomized, open-label clinical study was to compare the cardiovascular effects of sevoflurane and isoflurane via direct arterial blood pressure measurements and the lithium dilution cardiac output (LDCO) on premedicated healthy dogs undergoing elective tibial plateau leveling osteotomy (TPLO). Nineteen client-owned dogs were included. All dogs were premedicated with hydromorphone (0.05 mg/kg IV and glycopyrrolate 0.01 mg/kg subcutaneously). Ten dogs were anesthetized with sevoflurane and nine dogs were anesthetized with isoflurane. Eighteen dogs were instrumented with a dorsal pedal arterial catheter, and one dog had a femoral arterial catheter. All dogs had continuous, direct systolic (SAP), diastolic (DAP), and mean arterial (MAP) blood pressure readings as well as heart rate (HR), cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR), systemic vascular resistance index (SVRI), stroke volume variation (SVV), and pulse pressure variation (PPV) recorded q 5 min during the surgical procedure. There was no significant statistical difference in all parameters between the sevoflurane and isoflurane treatment groups. Both sevoflurane and isoflurane inhalant anesthetics appear to have similar hemodynamic effects when used as part of a multimodal anesthetic protocol in premedicated healthy dogs undergoing an elective surgical procedure.

Evaluation of the analgesic effects of diclofenac as a premedication drug in dogs undergoing ovariohysterectomy.

Pre-emptive analgesia consists of administering drugs such as opioids and nonsteroid anti-inflammatory drugs. This study aims to evaluate the intraoperative antinociceptive effects of diclofenac administered alone in premedication or combined with morphine along with its potential influence on recovery of dogs undergoing ovariohysterectomy. A total of 34 dogs (ASA I or II) admitted for ovariohysterectomy were randomly allocated into three groups according to the drugs given in premedication: Diclofenac (D) (n = 11), Morphine (M) (n = 13) and Diclofenac-Morphine (DM) (n = 10) groups. Induction and maintenance of anesthesia were standardized in all dogs. To assess intraoperative nociception, the heart rate (HR) and mean arterial pressure (MAP) were recorded during the surgery and at predefined time points: St (steady-state), Cut (cutaneous incision), P1 (first ovarian manipulation), P2 (second ovarian manipulation) and Cerv (cervical manipulation). The dynamic variation of HR (ΔHR) and MAP (ΔMAP) over 2 min was calculated at each time point. After extubation, early quality of recovery was assessed. Compared to St, a significant increase in HR and MAP at P1, P2 and Cerv was shown in all groups. MAP in the M group was lower at St than in the other groups. The dynamic variation of HR (ΔHR) and MAP (ΔMAP) was significantly less important at P2 and Cerv compared to P1 only in the DM group. Also, a better quality of recovery was shown in the D group compared to the M and DM groups. Diclofenac may be considered a suitable premedication drug and a part of a multimodal anesthetic approach in dogs.

Intranasal dexmedetomidine as premedication for magnetic resonance imaging examinations in dogs with neurological disorders mitigates hypotension and hypothermia.

OBJECTIVE: This study aimed to evaluate the safety and feasibility of intranasal administration of dexmedetomidine as a premedication for preventing hypotension and hypothermia in canine patients undergoing MRI examinations. ANIMALS: Dogs undergoing MRI examinations for neurological disorders were enrolled in this study. The dogs were randomly assigned: 15 to the N-Dex group (without premedication) and 13 to the Dex group (125 µg/m2 of dexmedetomidine, intranasally, as a premedication). METHODS: During the examination, pulse rate, systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure were recorded every 5 minutes for the first 30 minutes. Body temperature was measured before and after the examination. Any adverse events during the procedure were documented. RESULTS: Significant changes in pulse rate during the examination were not distinguishable. Although blood pressure and body temperature decreased in both groups under anesthesia, dogs in the Dex group had a significantly smaller drop in blood pressure and body temperature and fewer hypotension events than those in the N-Dex group MRI examinations of 1 hour's duration. Two dogs in the Dex group exhibited bradycardia at 45 and 60 minutes of MRI examination, which resolved after receiving atipamezole. CLINICAL RELEVANCE: Our results indicate that intranasal administration of 125 µg/m2 of dexmedetomidine as premedication is safe and can potentially mitigate hypothermia and hypotension in dogs with neurological disorders during MRI examinations.

The effect of age on the induction dose of propofol for general anesthesia in dogs.

OBJECTIVE: In people, the dose of propofol (DOP) required for procedural sedation and anesthesia decreases significantly with age. The objective of this study was to determine if the DOP required to perform endotracheal intubation decreases with age in dogs. STUDY DESIGN: Retrospective case series. ANIMALS: 1397 dogs. METHODS: Data from dogs anesthetized at referral center (2017-2020) were analyzed with three multivariate linear regression models with backward elimination using a combination of either absolute age, physiologic age, or life expectancy (ratio between age at the time of anesthetic event and expected age of death for each breed obtained from previous literature) as well as other factors as independent variables, and DOP as the dependent variable. The DOP for each quartile of life expectancy (<25%, 25-50%, 50-75%, 75-100%, >100%) was compared using one-way ANOVA. Significance was set at alpha = 0.025. RESULTS: Mean age was 7.2 ± 4.1 years, life expectancy 59.8 ± 33%, weight 19 ± 14 kg, and DOP 3.76 ± 1.8 mg kg-1. Among age models, only life expectancy was a predictor of DOP (-0.37 mg kg-1; P = 0.013) but of minimal clinical importance. The DOP by life age expectancy quartile was 3.9 ± 2.3, 3.8 ± 1.8, 3.6 ± 1.8, 3.7 ± 1.7, and 3.4 ± 1.6 mg kg-1, respectively (P = 0.20). Yorkshire Terrier, Chihuahua, Maltese, mixed breed dogs under 10 kg, and Shih Tzu required higher DOP. Status of neutered male, ASA E, and Boxer, Labrador and Golden Retriever breeds decreased DOP, along with certain premedication drugs. CONCLUSIONS AND CLINICAL RELEVANCE: In contrast to what is observed in people, an age cut-off predictive of DOP does not exist. Percentage of elapsed life expectancy along with other factors such as breed, premedication drug, emergency procedure, and reproductive status significantly alter DOP. In older dogs, the dose of propofol can be adjusted based on their elapsed life expectancy.