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

ObjectiveTo describe ketamine–propofol total intravenous anaesthesia (TIVA) following premedication with acepromazine and either medetomidine, midazolam or morphine in rabbits.Study designRandomized, crossover experimental study.AnimalsA total of six healthy female New Zealand White rabbits (2.2 ± 0.3 kg).MethodsRabbits 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.ResultsKetofol 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 relevancePremedication 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.     

Development of a sedation protocol using orally administered tiletamine–zolazepam–acepromazine in free-roaming dogs

Objective

To investigate the sedative effects in dogs of tiletamine–zolazepam–acepromazine (TZA) or ketamine–flunitrazepam (KF) administered orally and to evaluate the effectiveness of encapsulated TZA for capturing free-roaming dogs.

Cardiovascular effects of dobutamine,norepinephrine and phenylephrine in isoflurane-anaesthetized dogs administered dexmedetomidine–vatinoxan

ObjectiveTo determine whether dobutamine, norepinephrine or phenylephrine infusions alleviate hypotension in isoflurane-anaesthetized dogs administered dexmedetomidine with vatinoxan.Study designBalanced, randomized crossover trial.AnimalsA total of eight healthy Beagle dogs.MethodsEach dog was anaesthetized with isoflurane (end-tidal isoflurane 1.3%) and five treatments: dexmedetomidine hydrochloride (2.5 μg kg^–1) bolus followed by 0.9% saline infusion (DEX-S); dexmedetomidine and vatinoxan hydrochloride (100 μg kg^–1) bolus followed by an infusion of 0.9% saline (DEX-VAT-S), dobutamine (DEX-VAT-D), norepinephrine (DEX-VAT-N) or phenylephrine (DEX-VAT-P). The dexmedetomidine and vatinoxan boluses were administered at baseline (T0) and the treatment infusion was started after 15 minutes (T15) if mean arterial pressure (MAP) was < 90 mmHg. The treatment infusion rate was adjusted every 5 minutes as required. Systemic haemodynamics were recorded at T0 and 10 (T10) and 45 (T45) minutes. A repeated measures analysis of covariance model was used.ResultsMost dogs had a MAP < 70 mmHg at T0 before treatment. Treatments DEX-S and DEX-VAT all significantly increased MAP at T10, but systemic vascular resistance index (SVRI) was significantly higher and cardiac index (CI) lower after DEX-S than after DEX-VAT. CI did not significantly differ between DEX-S and DEX-VAT-S at T45, while SVRI remained higher with DEX-S. Normotension was achieved by all vasoactive infusions in every dog, whereas MAP was below baseline with DEX-VAT-S, and higher than baseline with DEX-S at T45. Median infusion rates were 3.75, 0.25 and 0.5 μg kg^–1 minute^–1 for dobutamine, norepinephrine and phenylephrine, respectively. Dobutamine and norepinephrine increased CI (mean ± standard deviation, 3.35 ± 0.70 and 3.97 ± 1.24 L minute^–1 m^–2, respectively) and decreased SVRI, whereas phenylephrine had the opposite effect (CI 2.13 ± 0.45 L minute^–1 m^–2).Conclusions and clinical relevanceHypotension in isoflurane-anaesthetized dogs administered dexmedetomidine and vatinoxan can be treated with either dobutamine or norepinephrine.     

Determination of the effective dosage of tiletamine–zolazepam–ketamine–xylazine,with or without methadone,in dogs

ObjectiveTo determine the effective dosage of the combination tiletamine–zolazepam–ketamine–xylazine (TKX), with or without methadone, in dogs.Study designProspective, randomized, experimental study.AnimalsA total of 29 dogs.MethodsDogs were randomly administered TKX (group TKX, n = 13) or combined with 0.3 mg kg^–1 of methadone (group TKXM, n = 16) intramuscularly. The TKX solution contained tiletamine (50 mg mL^–1), zolazepam (50 mg mL^–1), ketamine (80 mg mL^–1) and xylazine (20 mg mL^–1). The effective dosages for immobility in 50% and 95% of the population (ED₅₀ and ED₉₅) were estimated using the up-and-down method. Approximately 20 minutes after drug administration, a skin incision was performed and the response was judged as positive or negative if the dogs moved or did not move, respectively. The TKX volume for the subsequent dog in the same group was increased or decreased by 0.005 mL kg^–1 if the response of the previous dog was positive or negative, respectively. Heart and respiratory rates, and sedation/anesthesia scores (range 0–21) were recorded before and 15 minutes after drug administration.ResultsEstimated ED₅₀ and ED₉₅ (95% confidence intervals) were: TKX, 0.025 (0.020–0.029) and 0.026 (0.010–0.042) mL kg^–1; TKXM, 0.022 (0.018–0.025) and 0.033 (0.017–0.049) mL kg^–1. Median (interquartile range) scores for sedation/anesthesia were 17 (16–18) and 17 (15–20), and times until lateral recumbency were 5 (4–6) and 6 (4–10) minutes in TKX and TKXM, respectively (p > 0.05). In both groups heart and respiratory rates decreased, but values remained acceptable for anesthetized dogs.Conclusions and clinical relevanceThe results provide a guide for volumes of TKX and TKXM in dogs requiring restraint for minimally invasive procedures. Inclusion of methadone in the TKX combination did not influence ED₅₀.     

Behavioral and cardiopulmonary effects of dexmedetomidine–midazolam and dexmedetomidine–midazolam–butorphanol in the silver fox (Vulpes vulpes)

Objective

To evaluate the behavior and some cardiopulmonary variables of dexmedetomidine–midazolam or dexmedetomidine–midazolam-butor-phanol in the silver fox (Vulpes vulpes).

Effect of β-mannanase on the digestibility of diets with different protein sources in dogs determined by different methodologies

This experiment aimed at evaluating the effects of including the enzyme, β-mannanase, in dog (Canis lupus familiaris) diets based on either poultry (Gallus gallus domesticus) by-product meal (PBM) or soybean [Glycine max (L.) Merr.] Meal (SBM). The second objective was to evaluate 3 methods for determining energy and nutrient digestibility values in diets fed to dogs: total fecal collection (TFC) and use of aia or crude fiber (CF) as a marker. Eight dogs were allotted to a replicated latin square (4 by 4) design. There were 2 diets based on PBM as the major protein source and 2 diets based on SBM as the major protein source. Within each protein source, 1 diet contained no β-mannanase and 1 diet contained 0.01% β-mannanase. Diets were fed for an adaptation period of 5 d followed by 5 d of TFC. Fecal score (1 = watery feces to 5 = dry, hard pellets), pH, DM, and fecal volume were determined. The apparent total tract digestibility (ATTD) of DM, OM, CP, ether extract (EE), N-free extract (NFE), and GE, and ME content were calculated using the methods of TFC, AIA, and CF. Data were analyzed as a 2 by 2 by 3 split-split-plot design (β-mannanase, protein source, and digestibility calculation procedure). There were interactions between protein source and β-mannanase (P < 0.05). Supplementation of β-mannanase increased ATTD of nutrients and energy and ME (+ 195.3 kcal/kg) and also reduced fecal production in the diet with SBM, but not in the diet that contained PBM. There was an interaction between digestibility calculation procedure and protein source (P < 0.05). The use of AIA overestimated ATTD of the diets containing PBM, but digestibility values estimated based on TFC and CF were not different. Dogs fed diets containing SBM produced more feces with greater moisture content and lower pH compared with dogs fed the PBM diet (P < 0.05). Addition of 0.01% β-mannanase increased (P < 0.05) the digestibility and ME content of the diets containing SBM, but did not improve (P > 0.05) fecal texture. Results indicated that values for ATTD of energy and nutrients in diets containing sbm are not different if they are calculated based on TFC, AIA, or CF, but use of AIA may result in an overestimation of values for ATTD of energy and nutrients in diets containing PBM.     

Effect of phentolamine mesylate on regression of lidocaine–epinephrine epidural anaesthesia in sheep

ObjectiveTo determine the impact of epidural phentolamine on the duration of anaesthesia following epidural injection of lidocaine–epinephrine.Study designBlinded randomized experimental study.AnimalsA group of 12 adult ewes weighing 25.7 ± 2.3 kg and aged 8–9 months.MethodsAll sheep were administered epidural lidocaine (approximately 4 mg kg^–1) and epinephrine (5 μg mL^–1). Of these, six sheep were randomized into three epidural treatments, separated by 1 week, administered 30 minutes after lidocaine–epinephrine: SAL: normal saline, PHE1: phentolamine (1 mg) and PHE2: phentolamine (2 mg). The other six sheep were administered only epidural lidocaine–epinephrine: treatment LIDEP. Each injection was corrected to 5 mL using 0.9% saline. Noxious stimuli were pinpricks with a hypodermic needle and skin pinch with haemostatic forceps to determine the onset and duration of sensory and motor block. Heart rate, noninvasive mean arterial pressure (MAP), respiratory rate and rectal temperature were recorded.ResultsThe onset times were not different among treatments. Duration of sensory block was significantly shorter in SAL (57.5 ± 6.2 minutes), PHE1 (60.7 ± 9.0 minutes) and PHE2 (62.0 ± 6.7 minutes) than in LIDEP (81.7 ± 13.4 minutes) (p < 0.05). Duration of motor blockade was significantly shorter in PHE1 (59.4 ± 5.4 minutes) and PHE2 (54.3 ± 4.0 minutes) than in SAL (84.8 ± 7.0 minutes) and LIDEP (91.5 ± 18.2 minutes) (p < 0.01). MAP in PHE2 was decreased at 10 minutes after administration of phentolamine (p < 0.05).Conclusion and clinical relevanceEpidural administration of 5 mL normal saline after epidural injection of lidocaine–epinephrine reduced the duration of sensory but not motor block in sheep. Epidural administration of phentolamine diluted to the final volume of 5 mL diminished both the duration of sensory and motor block in sheep administered epidural lidocaine–epinephrine.     

Hepatitis in dogs. An indexed bibliography of journal articles (1994–2004)

Transmissible spongiform encephalopathies (TSEs) or prion diseases are unique disorders that are not caused by infectious micro-organisms (bacteria or fungi), viruses or parasites, but rather seem to be the result of an infectious protein. TSEs are comprised of fatal neurodegenerative disorders affecting both human and animals. Prion diseases cause sponge-like degeneration of neuronal tissue and include (among others) Creutzfeldt–Jacob disease in humans, bovine spongiform encephalopathy (BSE) in cattle and scrapie in sheep. TSEs are characterized by the formation and accumulation of transmissible (infectious) disease-associated protease-resistant prion protein (PrP^Sc), mainly in tissues of the central nervous system. The exact molecular processes behind the conversion of PrP^C into PrP^Sc are not clearly understood. Correlations between prion protein polymorphisms and disease have been found, however in what way these polymorphisms influence the conversion processes remains an enigma; is stabilization or destabilization of the prion protein the basis for a higher conversion propensity? Apart from the disease-associated polymorphisms of the prion protein, the molecular processes underlying conversion are not understood. There are some notions as to which regions of the prion protein are involved in refolding of PrP^C into PrP^Sc and where the most drastic structural changes take place. Direct interactions between PrP^C molecules and/or PrP^Sc are likely at the basis of conversion, however which specific amino acid domains are involved and to what extent these domains contribute to conversion resistance/sensitivity of the prion protein or the species barrier is still unknown.     

Effects of trilostane on the pituitary-adrenocortical and renin–aldosterone axis in dogs with pituitary-dependent hypercortisolism

The medical records of 63 dogs with pituitary-dependent hypercortisolism (PDH) before and during treatment with trilostane were reviewed retrospectively. The correct trilostane dosage in dogs with PDH was based on the resolution of clinical signs and the results of an adrenocorticotropic hormone (ACTH) stimulation test. The mean (±SD) dose rate of trilostane to achieve good clinical control was 2.8 ± 1.0 mg/kg bodyweight. Trilostane treatment resulted in a significant decline in basal plasma cortisol concentrations. The median plasma ACTH concentration (39 pmol/L, range 7–132 pmol/L; n = 60) at the optimal trilostane dosage time was significantly higher (P < 0.001) than before treatment (13 pmol/L, range 2–102 pmol/L). These values did not overlap with plasma ACTH concentrations (range 212–307 pmol/L) of five PDH dogs with trilostane-induced hypocortisolism.The median cortisol/ACTH ratio in well-controlled dogs (0.23, range 0.03–2.5; n = 46) was significantly lower (P < 0.001) than before treatment (2.59, range 0.27–13.25). Trilostane treatment resulted in an insignificant decrease in plasma aldosterone concentration (PAC), but the median plasma renin activity (PRA) at the time the trilostane dosage was considered optimal (265 fmol/L/s, range 70–3280 fmol/L/s; n = 18) was significantly higher (P < 0.001) than prior to treatment (115 fmol/L/s, range 15–1330 fmol/L/s). Similarly, the median PAC/PRA ratio during trilostane treatment (0.16, range 0.003–0.92; n = 17) was significantly lower (P < 0.001) than before treatment (median 0.44, range 0.04–1.33). Trilostane affected both the hypothalamic-pituitary-adrenocortical and the renin–aldosterone axes. The results also suggested that basal plasma ACTH concentration may be used to detect trilostane overdosage.     

Effects of intramuscular and intranasal administration of midazolam–dexmedetomidine on sedation and some cardiopulmonary variables in New Zealand White rabbits

ObjectiveTo compare the sedative and cardiopulmonary effects of intranasal (IN) and intramuscular (IM) administration of dexmedetomidine and midazolam combination in New Zealand White rabbits.Study designA randomized, crossover experimental study.AnimalsA total of eight healthy New Zealand White rabbits, aged 6–12 months, weighing 3.1 ± 0.3 kg (mean ± standard deviation).MethodsThe animals were randomly assigned to administration of dexmedetomidine (0.1 mg kg^–1) with midazolam (2 mg kg^–1) by either IN or IM route separated by 2 weeks. The electrocardiogram, pulse rate (PR), peripheral haemoglobin oxygen saturation (SpO₂), mean noninvasive arterial pressure (MAP), respiratory frequency (f_R) and rectal temperature were measured before drug administration (baseline), T₀ (onset of sedation) and at 5 minute intervals until recovery. The onset of sedation, duration of sedation and sedation score (SS) were also recorded.ResultsThe PR was significantly lower in treatment IM than in treatment IN over time (p = 0.027). MAP < 60 mmHg developed in two and four rabbits in treatments IN and IM, respectively. SpO₂ progressively decreased over time in both treatments. f_R was lower than baseline at several time points in both treatments. Onset of sedation was shorter in treatment IN (90 ± 21 seconds) than in treatment IM (300 ± 68 seconds) (p = 0.036). Duration of sedation was longer in treatment IM (55.2 ± 8.7 minutes) than in treatment IN (39.6 ± 2.1 minutes) (p = 0.047). No significant difference in SS was observed between treatments (p > 0.05).Conclusions and clinical relevanceCombination of dexmedetomidine (0.1 mg kg^–1) and midazolam (2 mg kg^–1) decreased f_R, PR and SpO₂ regardless of the administration route in New Zealand White rabbits. A more rapid action and shorter duration of sedation were observed after treatment IN than after treatment IM administration.     

Serosurvey of pathogens in domestic dogs on the border of No?l Kempff Mercado National Park, Bolivia.

The threat of disease transmission from domestic animals to wildlife has become recognized as an increasing concern within the wildlife community in recent years. Domestic dogs pose a significant risk as reservoirs for infectious diseases, especially for wild canids. As part of a multifaceted ecologic study of maned wolves and other canids in the large, remote No?l Kempff Mercado National Park (NKMNP) in northeastern Bolivia, 40 domestic dogs in two villages and at two smaller settlements bordering the national park were sampled for exposure to canine diseases. High levels of exposure were found to canine distemper virus and canine parvovirus, both of which are known to cause mortality in maned wolves and other carnivores. Moderate to high levels of exposure were found to rabies virus, Ehrlichia canis, and Toxoplasma gondii, as well as significant levels of infection with Dirofilaria immitis. This study reports evidence of exposure to several diseases in the domestic dogs bordering the park. Contact between wild carnivores and dogs has been documented in the sampled villages, therefore dogs likely pose a substantial risk to the carnivores within and near NKMNP. Further measures should be undertaken to decrease the risk of spillover infection from domestic animals into the wild species of this region.     

Effects of intracoelomic alfaxalone–dexmedetomidine on righting reflex in common garter snakes (Thamnophis sirtalis): preliminary data

ObjectiveTo evaluate the effect of dexmedetomidine on alfaxalone immobilization in snakes.Study designNonblinded, crossover study.AnimalsA total of eight mature common garter snakes (Thamnophis sirtalis).MethodsSnakes were administered each of three treatments intracoelomically: alfaxalone (30 mg kg^–1; treatment A), alfaxalone (30 mg kg^–1) combined with dexmedetomidine (0.05 mg kg^–1; treatment AD0.05); and alfaxalone (30 mg kg^–1) combined with dexmedetomidine (0.10 mg kg^–1; treatment AD0.10). A minimum of 10 days elapsed between experimental trials. Times to loss of righting reflex (LRR) and return of righting reflex (RRR) were recorded. Heart rate (HR) was recorded every 5 minutes throughout the period of LRR and averaged for each snake. Times to LRR and RRR, and mean HR in snakes that achieved LRR were reported.ResultsLRR occurred in eight (100%), five (63%) and three (38%) snakes in treatments A, AD0.05 and AD0.10, respectively. For all treatments, time to LRR ranged 3–20 minutes. Median (range) times to RRR were 39 (30–46), 89 (62–128) and 77 (30–185) minutes for treatments A, AD0.05 and AD0.10, respectively. In animals where righting reflex was lost, mean HR was lower in all dexmedetomidine treatments compared with treatment A.Conclusions and clinical relevanceIn this pilot study, alfaxalone resulted in reliable immobilization, whereas dexmedetomidine and alfaxalone combinations resulted in highly variable durations of immobilization with low HR in immobilized animals. For snakes that achieved LRR, the addition of dexmedetomidine (0.05 mg kg^–1) to alfaxalone appeared to extend the period of immobilization compared with alfaxalone alone.     

Effect of furosemide and furosemide–carbazochrome combination on exercise-induced pulmonary hemorrhage in Standardbred racehorses

The objective was to quantify the effect of furosemide and carbazochrome on exercise-induced pulmonary hemorrhage (EIPH) in Standardbred horses using red blood cell count and hemoglobin concentration in bronchoalveolar lavage (BAL) fluid. Six healthy Standardbred horses with prior evidence of EIPH performed a standardized treadmill test 4 h after administration of placebo, furosemide, or furosemide–carbazochrome combination. Red blood cell (RBC) counts and hemoglobin concentrations were determined on the BAL fluid. The RBC count in BAL ranges were (2903–26 025 cells/μL), (45–24 060 cells/μL), and (905–3045 cells/μL) for placebo, furosemide, and furosemide–carbazochrome, respectively. Hemoglobin concentration ranges were (0.03–0.59 mg/mL), (0.01–0.55 mg/mL), and (0.007–0.16 mg/mL) for placebo, furosemide, and furosemide– carbazochrome groups, respectively. No significant differences were detected among treatments. However, there was great variability among horses, suggesting that a larger sample size or better selection of horses was needed.