Neurophysiological assessment of the sedative and analgesic effects of a constant rate infusion of dexmedetomidine in the dog

The sedative and analgesic effects of continuous rate infusion (CRI) of dexmedetomidine (DEX) were investigated in Beagle dogs (n = 8) using auditory and somatosensory evoked potentials (AEPs and SEPs) recorded before, during and after a CRI of saline or DEX (1.0, 3.0, 5.0 μg/kg bolus, followed by 1.0, 3.0, 5.0 μg/kg/h CRI, respectively).The results showed a significant reduction in AEP at doses of 1.0 μg/kg/h and above and a significant reduction of the SEP at doses of 3.0 and 5.0 μg/kg/h. Neither the AEP nor the SEP was further reduced at 5.0 μg/kg/h when compared to 3.0 μg/kg/h, although a slower return towards baseline values was observed at 5.0 μg/kg/h. The mean plasma levels (±SEM) of DEX during infusion were 0.533 ± 0.053 ng/mL for the 1.0 μg/kg/h dose, 1.869 ± 0.063 ng/mL for the 3.0 μg/kg/h dose and 4.017 ± 0.385 for the 5.0 μg/kg/dose. It was concluded that in adult dogs, a CRI of DEX had a sedative and analgesic effect that could be described quantitatively using neurophysiological parameters. Sedation was achieved at lower plasma levels than required for analgesia, and DEX had a longer (but not larger) effect with infusion rates above 3.0 μg/kg/h.     

The effects of L-659,066, a peripheral alpha2-adrenoceptor antagonist, on dexmedetomidine-induced sedation and bradycardia in dogs

Objective  To investigate the influence of L-659,066, a peripheral α2-adrenoceptor antagonist, on dexmedetomidine-induced sedation and reduction in pulse rate (PR) in dogs.
Study design  Randomized, cross-over.
Animals  Six healthy laboratory Beagles.
Methods  All animals received dexmedetomidine (5 μg kg⁻¹ IV, DEX) alone or in combination with L-659,066 (250 μg kg⁻¹ IV, DEX + L) with a 7-day rest period between treatments. Sedation was assessed using a composite sedation score and PRs were recorded. Atipamezole (50 μg kg⁻¹ IM, ATI) was administered to reverse the sedation. Overnight Holter-monitoring was carried out to obtain a minimum heart rate (MHR) at rest.
Results  Bioequivalence was shown for clinical sedation between DEX and DEX + L. Heart rate was significantly higher with DEX + L during the period of sedation. Bioequivalence was demonstrated between MHR and PR in the DEX + L group during the period of sedation. Recoveries after ATI were uneventful.
Conclusions  L-659,066 did not affect the quality of dexmedetomidine-induced sedation whilst it attenuated the reduction in PR. Thus, L-659,066 could prove a useful adjunct to reduce the peripheral cardiovascular effects attributed to dexmedetomidine in dogs.
Clinical relevance  The clinical safety of α2-adrenoceptor agonists could be markedly improved with less peripheral cardiovascular effects.     

Sedative effects of propofol in horses

Objective  We hypothesized that propofol can produce rapidly-reversible, dose-dependent standing sedation in horses.
Study design  Prospective randomized, blinded, experimental trial.
Animals  Twelve healthy horses aged 12 ± 6 years (mean ± SD), weighing 565 ± 20 kg, and with an equal distribution of mares and geldings.
Methods  Propofol was administered as an intravenous bolus at one of three randomized doses (0.20, 0.35 and 0.50 mg kg⁻¹). Cardiovascular and behavioral measurements were made by a single investigator, who was blinded to treatment dose, at 3 minute intervals until subjective behavior scores returned to pre-sedation baseline values. Continuous data were analyzed over time using repeated-measures anova and noncontinuous data were analyzed using Friedman tests.
Results  There were no significant propofol dose or temporal effects on heart rate, respiratory rate, vertical head height, or jugular venous blood gases (pH_v, P_vO₂, P_vCO₂). The 0.35 mg kg⁻¹ dose caused mild sedation lasting up to 6 minutes. The 0.50 mg kg⁻¹ dose increased sedation depth and duration, but with increased ataxia and apparent muscle weakness.
Conclusions and clinical relevance  Intravenous 0.35 mg kg⁻¹ propofol provided brief, mild sedation in horses. Caution is warranted at higher doses due to increased risk of ataxia.     

Anaesthetic and cardiorespiratory effects of ketamine plus dexmedetomidine for chemical restraint in black capuchin monkeys (Sapajus nigritus)

AIMS: To evaluate the quality of anaesthesia and cardiorespiratory effects of ketamine and two doses of dexmedetomidine in captive black capuchin monkeys (Sapajus nigritus) undergoing routine clinical examination.

METHODS: Twenty-four animals undergoing routine clinical examination were enrolled in the study. Animals were briefly physically restrained and examined to ensure no obvious illness was present and that they were healthy. Monkeys were randomly allocated to two groups (n=12 per group) and then treated with a combination of I/M 7.5?mg/kg ketamine and either 30?µg/kg or 50?µg/kg dexmedetomidine (Dex30 or Dex50 groups, respectively). Interval to onset and duration of anaesthesia were recorded, and the quality of induction of anaesthesia and recovery were subjectively evaluated. Heart rate, respiratory rate, systolic arterial pressure (SAP), rectal temperature, degree of sedation, analgesia, muscle relaxation and response to auditory stimulus were measured every 5 minutes from onset of anaesthesia until recovery.

RESULTS: The mean interval to onset of anaesthesia was 7.3 (SD 6.6) and 9.1 (SD 5.0) minutes for the Dex30 and Dex50 groups, respectively (p=0.208). Mean duration of anaesthesia was longer for monkeys in the Dex50 (85.5 (SD 15.3) minutes) compared to those in Dex30 (63.9 (SD 16.4) minutes) group (p=0.003). Induction was considered excellent in 23/24 animals, and recovery was excellent in all animals. Heart rate, respiratory rate and body temperature decreased in both groups when compared to baseline, with no differences between groups. No differences between groups were found for assessments of sedation, analgesia, muscle relaxation or response to auditory stimulus.

CONCLUSION AND CLINICAL RELEVANCE: Administration of ketamine and dexmedetomidine at the two doses produced adequate, dose-dependent chemical restraint, with excellent induction and recovery, and minimal clinically significant cardiorespiratory effects in captive capuchin monkeys. Due to the occurrence of arrhythmias, electrocardiographic monitoring is recommended when this combination is used. The administration of higher doses of dexmedetomidine produced longer lasting anaesthesia without further compromise of cardiorespiratory parameters.     

Preliminary investigation of somatosensory evoked potentials in equine headshaking

The aim of this study was to develop a technique for recording electrical activity of the equine cerebral cortex following application of a noxious electrical stimulus to the maxillary branch of the trigeminal nerve in order to investigate trigeminal nerve neurophysiology in control and headshaking horses. Triphasic somatosensory evoked potentials (SEPs) were recorded using subcutaneous needle electrodes in four control and four headshaking horses under general anaesthesia. Dural electroencephalography electrodes were used to record SEPs in one further control and one further headshaking horse. Headshaking horses appeared to have decreased middle latency and inter-peak intervals following stimulation of the trigeminal nerve compared with control horses, supporting abnormal trigeminal nerve physiology in equine headshaking.     

Comparison of three doses of dexmedetomidine with medetomidine in cats following intramuscular administration

Cats ( n  = 6) were administered dexmedetomidine (DEX) and medetomidine (MED) at three different dose levels in a randomized, blinded, cross-over study. DEX was administered at 25, 50 and 75 μg/kg (D25, D50 and D75), corresponding to MED 50, 100 and 150 μg/kg (M50, M100 and M150). Sedation, analgesia and muscular relaxation were scored subjectively. Heart and respiratory rates and rectal temperature were measured. Corresponding doses of DEX and MED were compared. Effects were also compared between dose levels for each compound. At dose level 2 (D50-M100), the duration of effective clinical sedation was significantly shorter after DEX (202.5±16.0 min) than after MED (230.0±41.2 min). Proceeding from D50-M100 to D75-M150, the duration of effective clinical sedation was increased more after DEX (by 57.5±38.4 min) than after MED (by 14.2±41.9 min) Increasing from D50-M100 to D75-M150, heart rate was further decreased after DEX (by 8.1±13.4%) but not after MED. There was no statistically significant difference between corresponding doses of DEX and MED for any of the other parameters studied. Changes in sedation, analgesia and muscular relaxation were dose-dependent. It was concluded that anaesthetic effects of medetomidine in cats are probably due entirely to its d-isomer and that dexmedetomidine at 25, 50 and 75 μg/kg induces dose-dependent sedation, analgesia and muscular relaxation of clinical significance in cats.     

Clinical evaluation of the efficacy and safety of a constant rate infusion of dexmedetomidine for postoperative pain management in dogs

ObjectiveTo compare postoperative analgesia provided by a constant rate infusion (CRI) of dexmedetomidine (DMED) to that of a well-established positive control [morphine (MOR)] in critically ill dogs. The sedative, cardiorespiratory effects and clinical safety of a 24-hour DMED CRI were also evaluated.Study designProspective, randomised, blinded, positive-controlled parallel-group clinical study.AnimalsForty hospitalised, client-owned dogs requiring post-operative pain management after invasive surgery.MethodsAfter surgery, a loading dose of either DMED (25 μg m^?2) or MOR (2500 μg m^?2) followed by a 24-hour CRI of DMED (25 μg m^?2 hour^?1) or MOR (2500 μg m^?2 hour^?1) was administered. Pain was measured using the Short Form of the Glasgow Composite Measure Pain Scale, sedation and physiological variables were scored at regular intervals. Animals considered to be painful received rescue analgesia and were allocated to a post-rescue protocol; animals which were unresponsive to rescue analgesia were removed from the study. Data were analysed with anova, two-sample t-tests or Chi-square tests. Time to intervention was analysed with Kaplan–Meier methodology.ResultsForty dogs were enrolled. Twenty dogs (9 DMED and 11 MOR) did not require rescue analgesia. Eleven DMED and eight MOR dogs were allocated to the post-rescue protocol and seven of these removed from the study. Significant differences in pain scores between groups were not observed during the first 12 hours, however, DMED dogs were less (p = 0.009) painful during the last 12 hours. Sedation score over the entire 24-hour study was not significantly different between groups.Conclusion / Clinical RelevanceDexmedetomidine CRI was equally effective as MOR CRI at providing postoperative analgesia and no clinically significant adverse reactions were noted. This study shows the potential of DMED to contribute to a balanced postoperative analgesia regimen in dogs.     

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.     

Somatosensory evoked potentials produced by stimulation of the dorsomedial nerves innervating the tail in dogs

To record the somatosensory evoked potentials (SEPs) produced by stimulation of tail nerves and determine the effects of acute compression of the cauda equina on SEPs. The subjects were 10 adult Beagles. SEPs were recorded after stimulating the dorsomedial nerves (DMN) innervating the tail. The cauda equina was compressed using a balloon catheter inserted into the vertebral arch. In SEPs, two negative and one positive peak were often observed. The compression of the cauda equina caused significant depression of the positive component. The SEPs produced by stimulation of the DMN reflect the activities of ascending neuronal pathways above the coccygeal spinal segments and may be a useful tool for examining cauda equina syndrome.     

Comparative study on the sedative effects of morphine, methadone, butorphanol or tramadol, in combination with acepromazine, in dogs

Objective  To compare the effects of morphine (MOR), methadone (MET), butorphanol (BUT) and tramadol (TRA), in combination with acepromazine, on sedation, cardiorespiratory variables, body temperature and incidence of emesis in dogs.
Study design  Prospective randomized, blinded, experimental trial.
Animals  Six adult mixed-breed male dogs weighing 12.0 ± 4.3 kg.
Methods  Dogs received intravenous administration (IV) of acepromazine (0.05 mg kg⁻¹) and 15 minutes later, one of four opioids was randomly administered IV in a cross-over design, with at least 1-week intervals. Dogs then received MOR 0.5 mg kg⁻¹; MET 0.5 mg kg⁻¹; BUT 0.15 mg kg⁻¹; or TRA 2.0 mg kg⁻¹. Indirect systolic arterial pressure (SAP), heart rate (HR), respiratory rate ( f _R), rectal temperature, pedal withdrawal reflex and sedation were evaluated at regular intervals for 90 minutes.
Results  Acepromazine administration decreased SAP, HR and temperature and produced mild sedation. All opioids further decreased temperature and MOR, BUT and TRA were associated with further decreases in HR. Tramadol decreased SAP whereas BUT decreased f _R compared with values before opioid administration. Retching was observed in five of six dogs and vomiting occurred in one dog in MOR, but not in any dog in the remaining treatments. Sedation scores were greater in MET followed by MOR and BUT. Tramadol was associated with minor changes in sedation produced by acepromazine alone.
Conclusions and clinical relevance  When used with acepromazine, MET appears to provide better sedation than MOR, BUT and TRA. If vomiting is to be avoided, MET, BUT and TRA may be better options than MOR.     

Constant rate infusion of ketamine reduces minimal alveolar concentration of isoflurane in alpacas

Ketamine is a rapid acting, potent, nonspecific, noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist commonly used for inducing general anesthesia and for providing post-operative pain management and may possibly lessen the need for other potentially harmful or contraindicated analgesics in camelids, such as nonsteroidal anti-inflammatory drugs. Prior to determining the effectiveness of CRI ketamine for analgesia, a safe, sub-anesthetic dose was established that did not produce untoward side effects, sedation or alter normal behavior. Six healthy male alpacas (40–90 kg) were used for the trial and each acted as its own control. Each alpaca was randomly assigned to receive ketamine at 20 and 40 μg kg^–1 minute^–1 in 500 mL saline. A blinded observer recorded heart rate, respiratory rate, and body temperature hourly, and behavior for 8 hours. There was a 72-hour washout period between each dosing regime. An equal volume saline CRI without ketamine was used as a control. Each alpaca was allowed a one-week washout prior to being anesthetized with isoflurane using mask induction. After achieving a stable plane of anesthesia, the MAC value for isoflurane was determined. Ketamine was infused at 40 μg kg^–1pre-existing pain is unknown, but for elective procedures, preemptive analgesia using ketamine CRI in alpacas may be beneficial.     

Thermal antinociception after dexmedetomidine administration in cats: a dose-finding study

The optimum dose of dexmedetomidine for antinociception to a thermal stimulus was determined in a crossover study of 12 cats. In five treatment groups ( n  = 10 per group), dexmedetomidine was administered intramuscularly (i.m.) at 2, 5, 10, 20 and 40 μg/kg; positive and negative controls were administered buprenorphine (20 μg/kg, i.m.) and 0.9% saline (0.006 mL/kg, i.m.) respectively. Baseline thermal thresholds and visual analogue scale (VAS) sedation scores were obtained prior to drug treatment and then at regular intervals until 24 h after administration. The summary measures of overall mean thresholds and overall mean VAS scores were investigated using a univariate general linear model for multiple factors with post hoc Tukey's tests ( P  < 0.05). Only dexmedetomidine at 40 μg/kg displayed an analgesic effect (less than that of buprenorphine). The VAS for sedation did not significantly affect the thresholds obtained and treatment was the only significant factor to influence VAS. Dexmedetomidine resulted in higher VAS for sedation than saline and buprenorphine. Dexmedetomidine at 40 μg/kg significantly increased nociceptive thresholds compared with saline control, but less than buprenorphine. Dexmedetomidine produced dose-dependent sedation, but only the highest dose produced analgesia, suggesting that induction of analgesia requires the highest dose (or an additional analgesic) in the clinical setting.     

Effect of lidocaine on the minimum alveolar concentration of sevoflurane in dogs

Objective  To investigate the effects of a low-dose constant rate infusion (LCRI; 50 μg kg⁻¹ minute⁻¹) and high-dose CRI (HCRI; 200 μg kg⁻¹ minute⁻¹) lidocaine on arterial blood pressure and on the minimum alveolar concentration (MAC) of sevoflurane (Sevo), in dogs.
Study design  Prospective, randomized experimental design.
Animals  Eight healthy adult spayed female dogs, weighing 16.0 ± 2.1 kg.
Methods  Each dog was anesthetized with sevoflurane in oxygen and mechanically ventilated, on three separate occasions 7 days apart. Following a 40-minute equilibration period, a 0.1-mL kg⁻¹ saline loading dose or lidocaine (2 mg kg⁻¹ intravenously) was administered over 3 minutes, followed by saline CRI or lidocaine LCRI or HCRI. The sevoflurane MAC was determined using a tail clamp. Heart rate (HR), blood pressure and plasma concentration of lidocaine were measured. All values are expressed as mean ± SD.
Results  The MAC of Sevo was 2.30 ± 0.19%. The LCRI reduced MAC by 15% to 1.95 ± 0.23% and HCRI by 37% to 1.45 ± 0.21%. Diastolic and mean pressure increased with HCRI. Lidocaine plasma concentration was 0.84 ± 0.18 for LCRI and 1.89 ± 0.37 μg mL⁻¹ for HCRI. Seventy-five percent of HCRI dogs vomited during recovery.
Conclusion and clinical relevance  Lidocaine infusions dose dependently decreased the MAC of Sevo, did not induce clinically significant changes in HR or arterial blood pressure, but vomiting was common during recovery in HCRI.     

Sedative effect of detomidine in infant calves.

Detomidine administered intramuscularly at a dose of 10, 20 or 40 micrograms/kg body mass was evaluated for its sedative effects in 15 unfasted infant calves (age: 15-20 days; body mass: 18-33 kg). The drug produced dose-dependent sedation. At a dose of 10 micrograms/kg detomidine produced effective sedation for 30 to 45 min without any observable analgesia. At doses of 20 or 40 micrograms/kg it caused deep sedation, sternal recumbency, and moderate analgesia of the trunk. Hyperglycaemia was recorded at all dose levels. The changes in respiratory rate, rectal temperature, haemoglobin, packed cell volume, total erythrocyte count and plasma concentration of total protein were not significant.     

Effects of different doses of L-659'066 on the bispectral index and clinical sedation in dogs treated with dexmedetomidine

ObjectiveTo evaluate the effects of three doses of L-659’066 (MK-467) on the bispectral index (BIS) and clinical sedation in dexmedetomidine-sedated Beagles.Study designRandomized, experimental cross over study.AnimalsEight purpose-bred healthy laboratory Beagles.MethodsDexmedetomidine (10 μg kg^?1 IV [DEX]) was administered alone or in combination with three doses of L-659’066 (250 μg kg^?1 [DL250]; 500 μg kg^?1 [DL500] and 750 μg kg^?1 [DL750] IV) in the same syringe in a randomized crossover manner. The bispectral index (BIS), electromyography (EMG) and sedation score were recorded at baseline and 5, 10, 20, 30, 45 and 60 minutes after treatment.ResultsWhen compared to DEX, BIS and EMG were significantly higher and the sedation score significantly lower with DL500 and DL750. With DEX, BIS was significantly decreased at times 20, 30 and 60 minutes whereas the sedation scores were significantly increased at all time points after drug administration in all groups. Bioequivalence for clinical sedation was detected between DEX and all doses of L-659’066, reaching European Medicines Agency (EMA) standards.Conclusions and clinical relevanceAlthough L-659’066 interfered with dexmedetomidine induced sedation, the degree of the reduction was not clinically relevant. Despite performing better when dexmedetomidine was used alone, BIS did not reflect the clinical sedative status when the antagonist was added.     

Postoperative analgesic effects of either a constant rate infusion of fentanyl,lidocaine, ketamine,dexmedetomidine, or the combination lidocaine‐ketamine‐dexmedetomidine after ovariohysterectomy in dogs

ObjectiveTo evaluate the postoperative analgesic effects of a constant rate infusion (CRI) of either fentanyl (FENT), lidocaine (LIDO), ketamine (KET), dexmedetomidine (DEX), or the combination lidocaine-ketamine-dexmedetomidine (LKD) in dogs.Study designRandomized, prospective, blinded, clinical study.AnimalsFifty-four dogs.MethodsAnesthesia was induced with propofol and maintained with isoflurane. Treatments were intravenous (IV) administration of a bolus at start of anesthesia, followed by an IV CRI until the end of anesthesia, then a CRI at a decreased dose for a further 4 hours: CONTROL/BUT (butorphanol 0.4 mg kg⁻¹, infusion rate of saline 0.9% 2 mLkg⁻¹ hour⁻¹); FENT (5 μg kg⁻¹, 10 μg kg⁻¹hour⁻¹, then 2.5 μg kg⁻¹ hour⁻¹); KET (1 mgkg⁻¹, 40 μg kg⁻¹ minute⁻¹, then 10 μg kg⁻¹minute⁻¹); LIDO (2 mg kg⁻¹, 100 μg kg⁻¹ minute⁻¹, then 25 μg kg⁻¹ minute⁻¹); DEX (1 μgkg⁻¹, 3 μg kg⁻¹ hour⁻¹, then 1 μg kg⁻¹ hour⁻¹); or a combination of LKD at the aforementioned doses. Postoperative analgesia was evaluated using the Glasgow composite pain scale, University of Melbourne pain scale, and numerical rating scale. Rescue analgesia was morphine and carprofen. Data were analyzed using Friedman or Kruskal–Wallis test with appropriate post-hoc testing (p < 0.05).ResultsAnimals requiring rescue analgesia included CONTROL/BUT (n = 8), KET (n = 3), DEX (n = 2), and LIDO (n = 2); significantly higher in CONTROL/BUT than other groups. No dogs in LKD and FENT groups received rescue analgesia. CONTROL/BUT pain scores were significantly higher at 1 hour than FENT, DEX and LKD, but not than KET or LIDO. Fentanyl and LKD sedation scores were higher than CONTROL/BUT at 1 hour.Conclusions and clinical relevanceLKD and FENT resulted in adequate postoperative analgesia. LIDO, CONTROL/BUT, KET and DEX may not be effective for treatment of postoperative pain in dogs undergoing ovariohysterectomy.     

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.     

Effect of stunning on spontaneous physical activity and evoked activity in the brain

1. The effect of stunning current on the time to recovery of physical activity, and on somatosensory evoked potentials (SEPs) in the brain, was examined in broiler chickens. 2. Increasing stunning current was associated with an increase in the time to recovery of tension in the neck muscles and with an increase in the incidence of loss of SEPs. 3. Currents greater than 105 mA per bird provided 52 s or more of apparent insensibility; currents greater than 120 mA were associated with absence of SEPs following the stun.     

Effect of electrical stunning on somatosensory evoked potentials in chickens

The spontaneous EEG and somatosensory evoked potentials (SEPs) were examined in chickens before and after electrical stunning using a waterbath stunner. Fifty-four per cent of the birds became epileptic and lost their SEPs, and 17% were non-epileptic and appeared to retain their SEPs. It was concluded that there was a reasonably close association between the presence of epileptiform activity in the EEG and the absence of SEPs following electrical stunning, but that the absence of SEPs could be preferred as an indicator of an effective stun on conceptual grounds.