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.     

The effect of medetomidine premedication upon propofol induction and infusion anaesthesia in the dog

The effect of premedication with four different intramuscular doses of medetomidine (5.0,10.0, 20.0 and 40.0 μg.kg-¹) and a saline placebo were compared in a group of six adult beagle dogs anaesthetised with propofol on five separate occasions. Anaesthesia was induced 30 minutes after premedication and maintained by intravenous injection and continuous infusion of propofol. The effects of medetomidine were reversed with atipamezole 30 minutes after anaesthetic induction. The marked synergistic effects of medetomidine with propofol were demonstrated by a dose related reduction in the induction and infusion requirements for a similar degree of anaesthesia. The effect appeared exponential in nature; lower medetomidine doses produced a disproportionately greater effect.
The maintenance of anaesthesia with propofol following a saline placebo or low doses of medetomidine proved to be difficult. Higher doses of medetomidine required less propofol for induction and infusion and allowed a more stable anaesthesia to be maintained. Propofol produced no statistically significant change in heart rate during infusion. Changes in respiratory rate were markedly group specific. A significant reduction in respiratory rate was seen in dogs given either 5 μg.kg- or 10 μ-g.kg-¹ medetomidine. No change was recorded in dogs given 20 /μg.kg-¹ medetomidine and a significant increase was seen in dogs given 40 μg.kg-¹ medetomidine. Recovery was monitored following the termination of propofol infusion after the reversal of medetomidine using atipamezole at five times the medetomidine dose. Recovery was slower for dogs given lower doses of medetomidine and consequently higher doses of propofol.     

Prothrombotic and Inflammatory Effects of Intravenous Administration of Human Immunoglobulin G in Dogs

Background: Intravenous administration of human immunoglobulin G (hIVIgG) has been suggested to potentiate thromboembolism in dogs, but supportive scientific reports are lacking.
Objectives: To determine if hIVIgG therapy promotes hypercoagulability and inflammation in dogs.
Animals: Twelve healthy Beagle dogs.
Methods: Prospective, experimental trial. An hIVIgG/saline solution was infused IV at 1 g/kg BW over 8 hours to 6 dogs, and physiological saline was infused to the other 6 dogs. Blood samples were drawn before, during, and after infusion for serial measurement of indicators of coagulation and inflammation. Data were analyzed by 2-way repeated measures analysis of variance.
Results: Dogs administered hIVIgG developed mildly decreased blood platelet concentrations without thrombocytopenia (median, 200 × 10³/μL; range, 150–302 × 10³/μL; P < .01), leukopenia (median, 3.5 × 10³/μL; range, 20–62 × 10³/μL; P < .001), and mildly increased plasma total protein concentrations (median, 6.3 g/dL; range, 5.6–6.7 g/dL; P < .001). Administration of hIVIgG was also associated with increases in fibrin/fibrinogen degradation products in all dogs (either 5 μg/mL or 10 μg/dL), thrombin-antithrombin III complexes (median, 7.2 ng/mL; range, 4.9–14.2 ng/mL; P < .001), and C-reactive protein concentrations (median, 2.5 mg/dL; range, 0.5–4.3 mg/dL; P < .01).
Conclusion and Clinical Importance: Administration of hIVIgG to dogs promotes hypercoagulability and an inflammatory state. This should be further evaluated and considered when using hIVIgG in dogs with IMHA or other prothrombotic conditions.     

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.     

Comparison of opioid and alpha-2 adrenergic receptor location and density in the horse and dog using radioligand binding

Ketamine, a noncompetitive NMDA receptor antagonist, has been shown to provide analgesia in some species. To target the NMDA receptor specifically and to potentially minimize some untoward side-effects, ketamine had been used epidurally. The objective of this study was to determine the analgesic effect of epidurally administered ketamine in dogs with chemically induced synovitis.
Sixteen healthy dogs were used. Dogs were anesthetized with propofol (4 mg kg⁻¹ IV). Synovitis was induced by injecting 1 mL of sodium urate crystal solution (10 mg mL⁻¹) into the right stifle. Dogs were allowed to recover and the synovitis was allowed to develop for 12 hours. The dogs were then anesthetized again using propofol (4 mg kg⁻¹ IV). Lumbosacral epidural injections were performed with each dog receiving either 2 mg kg⁻¹ of ketamine (20 mg mL⁻¹) or an equal volume of placebo (sterile water containing not more than 0.1 mg mL⁻¹ benzethonium chloride). Analgesia was assessed at baseline and then at 12, 14, 16, 18, 20, and 24 hours after induction of synovitis. Ground reaction forces (peak vertical force and impulse area) and overall pain were measured using a force platform and a pain scoring system (numerical rating scale).
Analysis of the data by Repeated Measures anova showed that the dogs developed a significant lameness between the baseline and 12 hours. However, no significant difference in ground reaction forces or total pain score was demonstrated between the treatment and control groups at any other time.
In conclusion, ketamine administered epidurally at a dose of 2 mg kg⁻¹ did not provide significant analgesia in dogs with chemically induced synovitis.     

A step towards effect-site target-controlled infusion with propofol in dogs: a ke0 for propofol

Target-controlled infusion (TCI) anesthesia using target effect-site concentration rather than plasma concentration provides less drug consumption, safer anesthesia, less undesired side effects and improved animal welfare. The aim of this study was to calculate the constant that converts propofol plasma into effect-site concentration ( k _e0) in dogs, and to implement it in a TCI system and compare it with the effect on the central nervous system (CNS). All dogs were subjected to general anesthesia using propofol. Fourteen dogs were used as the pilot group to calculate k _e0, using the t _peak method. Fourteen dogs were used as the test group to test and validate the model. R ugloop ii ^® software was used to drive the propofol syringe pump and to collect data from S/5 Datex monitor and cerebral state monitor. The calculated k _e0 was incorporated in an existing pharmacokinetic model (Beths Model). The relationship between propofol effect site concentrations and anesthetic planes, and propofol plasma and effect-site concentrations was compared using Pearson's correlation analysis. Average t _peak was 3.1 min resulting in a k _e0 of 0.7230 min⁻¹. The test group showed a positive correlation between anesthetic planes and propofol effect-site concentration ( R  = 0.69; P <  0.0001). This study proposes a k _e0 for propofol with results that demonstrated a good adequacy for the pharmacokinetic model and the measured effect. The use of this k _e0 will allow an easier propofol titration according to the anesthetic depth, which may lead to a reduction in propofol consumption and less undesired side effects usually associated to high propofol concentrations in dogs.     

The effect of pre-anaesthetic medication on the incidence of cardiac arrhythmias during halothane anaesthesia in cats

Objective To compare the incidence of arrhythmias in cats receiving either acepromazine or diazepam for pre-anaesthetic medication prior to halothane anaesthesia.
Study design A blinded, randomized clinical study.
Animals Forty-six healthy cats undergoing surgery.
Methods Animals were allocated to one of two groups for pre-anaesthetic medication. Group 1 received diazepam (0.2 mg kg⁻¹). Group 2 received acepromazine (0.02 mg kg⁻¹). The trial drug was administered intramuscularly in combination with buprenorphine (0.01 mg kg⁻¹) 30 minutes prior to induction of anaesthesia with propofol (approximately 5 mg kg⁻¹). Anaesthesia was maintained using halothane: delivered concentration was 1–2% carried in oxygen and nitrous oxide via an endotracheal tube attached to an Ayre's T-piece (with Jackson-Rees modification) breathing system. The incidence of cardiac arrhythmias was determined by continuously monitoring the electrocardiogram from the time of induction until recovery occurred. Demographical group characteristics were compared using analysis of variance. The incidence of cardiac arrhythmias was compared by the Chi squared test. Statistical significance was set at the 5% level.
Results The two groups were similar in weight, age, length and type of procedure undertaken. The incidence of arrhythmias was the same in each group (3/23 cases) ( p = 1.0).
Conclusions The incidence of cardiac arrhythmias in this study did not appear to be influenced by the nature of pre-anaesthetic medication.
Clinical relevance The incidence of cardiac arrhythmias under halothane anaesthesia was 13% in this study. Acepromazine did not appear to exert an anti-arrhythmic effect. This may not be the case in a larger scale study.     

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.     

Effects of diazepam, ketamine, and their combination on intraocular pressure in normal dogs

Ketamine has been implicated as causing increases in intraocular pressure. The purpose of this study is to document the effects of ketamine, diazepam, and their combination on intraocular pressure (IOP) in normal, unpremedicated dogs. Random-source dogs were assigned to one of five groups of 10 dogs each: ketamine 5 mg kg^–1 (KET5), ketamine 10 mg kg^–1 (KET10), diazepam 0.5 mg kg^–1 (VAL), ketamine 10 mg kg^–1 with diazepam 0.5 mg kg^–1 (KETVAL), saline 0.1 mL kg^–1 (SAL), all given intravenously. A baseline IOP was measured before injection, immediately after injection, and at 5, 10, 15, and 20 minutes following injection. IOP was increased over baseline immediately after injection in the KET5, KET10, and KETVAL groups; at 5, 10, and 15 minutes in the KET5 group; and at 20 minutes in the KETVAL group. The mean IOP change compared to SAL increased immediately after injection and at 5 minutes in the KET5, KET10, and KETVAL groups; at 10 and 15 minutes in the KET5 group, and at 20 minutes in the KETVAL group. The mean IOP increased up to 5.7, 3.2, and 3.1 mm Hg over mean baseline in the KET5, KET10, and KETVAL groups, respectively. All dogs in the KET5 group and the majority in the KETVAL and KET10 groups had an increase in their IOP over baseline. Ketamine caused a clinically and statistically significant elevation in IOP over baseline and compared to SAL. The concurrent addition of diazepam did not blunt this increase. Ketamine should be avoided in dogs with corneal trauma, glaucoma, or in those undergoing intraocular surgery.     

Cardiopulmonary and isoflurane‐sparing effects of epidural or intravenous infusion of dexmedetomidine in cats undergoing surgery with epidural lidocaine

ObjectiveTo compare the cardiorespiratory, anesthetic-sparing effects and quality of anesthetic recovery after epidural and constant rate intravenous (IV) infusion of dexmedetomidine (DEX) in cats given a low dose of epidural lidocaine under propofol-isoflurane anesthesia and submitted to elective ovariohysterectomy.Study designRandomized, blinded clinical trial.AnimalsTwenty-one adult female cats (mean body weight: 3.1 ± 0.4 kg).MethodsCats received DEX (4 μg kg^?1, IM). Fifteen minutes later, anesthesia was induced with propofol and maintained with isoflurane. Cats were divided into three groups. In GI cats received epidural lidocaine (1 mg kg^?1, n = 7), in GII cats were given epidural lidocaine (1 mg kg^?1) + DEX (4 μg kg^?1, n = 7), and in GIII cats were given epidural lidocaine (1 mg kg^?1) + IV constant rate infusion (CRI) of DEX (0.25 μg kg^?1 minute^?1, n = 7). Variables evaluated included heart rate (HR), respiratory rate (f_R), systemic arterial pressures, rectal temperature (RT), end-tidal CO₂, end-tidal isoflurane concentration (e′ISO), arterial blood gases, and muscle tone. Anesthetic recovery was compared among groups by evaluation of times to recovery, HR, f_R, RT, and degree of analgesia. A paired t-test was used to evaluate pre-medication variables and blood gases within groups. anova was used to compare parametric data, whereas Friedman test was used to compare muscle relaxation.ResultsEpidural and CRI of DEX reduced HR during anesthesia maintenance. Mean ± SD e′ISO ranged from 0.86 ± 0.28% to 1.91 ± 0.63% in GI, from 0.70 ± 0.12% to 0.97 ± 0.20% in GII, and from 0.69 ± 0.12% to 1.17 ± 0.25% in GIII. Cats in GII and GIII had longer recovery periods than in GI.Conclusions and clinical relevanceEpidural and CRI of DEX significantly decreased isoflurane consumption and resulted in recovery of better quality and longer duration, despite bradycardia, without changes in systemic blood pressure.     

Plasma and urine disposition and dose proportionality of ceftiofur and metabolites in dogs after subcutaneous administration of ceftiofur sodium

Nine male dogs (10.3–13.5 kg body weight) were randomly assigned to three groups of three dogs each and administered ceftiofur sodium subcutaneously as a single dose of 0.22, 2.2, or 4.4 mg ceftiofur free acid equivalents/kg body weight. Plasma and urine samples were collected serially for 72 h and assayed for ceftiofur and metabolites (derivatized to desfuroylceftiofur acetamide) using high-performance liquid chromatography. Urine concentrations remained above the MIC ₉₀ for Escherichia coll (4.0 μg/mL) and Proteus mirabilis (1.0 μg/mL) for over 24 h after doses of 2.2 mg/kg (8.1 μg/mL) and 4.4 mg/kg (29.6 μg/mL), the interval between treatments for ceftiofur sodium in dogs, whereas urine concentrations 24 h after dosing at 0.22 mg/kg (0.1 mg/Ib) were below the MIC ₉₀ for E.coli and P. mirabills (0.6 μg/mL). Plasma concentrations were dose-proportional, with peak concentrations of 1.66 ± 0.0990 μg/mL, 8.91 ± 6.42 μg/mL, and 26.7 ± 1.07 μg/mL after doses of 0.22, 2.2, and 4.4 mg/kg, respectively. The area under the plasma concentration versus time curve, when normalized to dose, was similar across all dosage groups.     

Cytosine Arabinoside as a Single Agent for the Induction of Remission in Canine Lymphoma

Cytosine arabinoside (AraC) was administered as a continuous IV infusion to 15 dogs with malignant lymphoma at a dose of 300 mg/m²/d for 2 consecutive days. Dogs were re-examined 7 d after treatment for response to therapy and for hematologic toxicity. Regardless of response, all dogs were started on combination chemotherapy at this time. Other toxicities were reported by owners. No dog responded objectively to Ara-C treatment, although 1 dog with circulating lymphoblasts had partial regression of lymphadenopathy but persistent blastemia. Thrombocytopenia (platelet count < 200,000/μL) 7 days posttreatment was the most commonly encountered hematologic toxicity, occurring in 10 of 14 dogs. Three of these 10 dogs were also mildly neutropenic (neutrophil counts of 2000 to 3000 cell/μL). Nonhematologic toxicity occurred in 8 of 15 dogs and was principally gastrointestinal in nature and mild in severity. Cytosine arabinoside at a dose of 300 mg/m²/day was not considered an active drug for the induction of remission in dogs with lymphoma.     

Evaluation of the Perkins® handheld applanation tonometer in the measurement of intraocular pressure in dogs and cats

Objective  To evaluate and to validate the accuracy of the Perkins^® handheld applanation tonometer in the measurement of IOP in dogs and cats.
Animals  Twenty eyes from 10 dogs and 10 cats immediately after sacrifice were used for the postmortem study and 20 eyes from 10 clinically normal and anesthetized dogs and cats were used for the in vivo study. Both eyes of 20 conscious dogs and cats were also evaluated.
Procedure  Readings of IOP postmortem and in vivo were taken using manometry (measured with a mercury column manometer) and tonometry (measured with a Perkins^® handheld applanation tonometer). The IOP measurement with Perkins^® tonometer in anesthetized and conscious dogs and cats was accomplished by instillation of proxymetacaine 0.5% and of 1% fluorescein eye drops.
Results  The correlation coefficient ( r ²) between the manometry and the Perkins^® tonometer were 0.982 (dogs) and 0.988 (cats), and the corresponding linear regression equation were y  = 0.0893 x  + 0.1105 (dogs) and y  = 0.0899 x  + 0.1145 (cats) in the postmortem study. The mean IOP readings with the Perkins^® tonometer after calibration curve correction were 14.9 ± 1.6 mmHg (range 12.2–17.2 mmHg) in conscious dogs, and were 15.1 ± 1.7 mmHg (range 12.1–18.7 mmHg) in conscious cats.
Conclusion  There was an excellent correlation between the IOP values obtained from direct ocular manometry and the Perkins^® tonometer in dogs and cats. The Perkins^® handheld tonometer could be in the future a new alternative for the diagnosis of glaucoma in veterinary ophthalmology.     

Comparison between S(+) ketamine–diazepam and S(+) ketamine–midazolam on anesthetic induction and recovery in dogs

S(+) ketamine, one of the two enantiomers of racemic ketamine, is a phencyclidine derivative that induces amnesia and analgesia. Its activity is related to blockade of NMDA receptors and some opioid action. We compared anesthetic induction and recovery quality with S(+) ketamine in combination with diazepam or midazolam in 10 dogs (ASA 1) admitted for elective surgery. After all clinical examinations, the dogs were separated into two groups (G I and G II). All animals received acepromazine (0.1 mg kg^?1) and fentanyl (5 µg kg^?1) IM, 20 minutes before induction with S(+) ketamine (6 mg kg^?1) and diazepam (0.5 mg kg^?1) IV (G I) or midazolam 0.2 mg kg^?1 (G II) IV. The doses of diazepam and midazolam were chosen according to the literature. All dogs were intubated and then maintained with halothane in oxygen at a vaporizer setting sufficient to maintain surgical anesthesia. Quality of induction, time needed for intubation, heart rate, respiratory rate, SpO₂, time to extubation, and quality of recovery were evaluated. The results were analyzed by Student's t‐test. Smooth induction and recovery were observed in all animals. The time to intubation was 45 ± 20 (GI) and 25 ± 6 seconds (GII), HR was 122 ± 12 (GI) and 125 ± 7 beats minute^?1 (GII), RR was 17 ± 2 (GI) and 21 ± 3 breaths minute^?1 (GII), SpO₂ was 96 ± 2 (GI) and 94 ± 1% (GII), time to extubation was 7 ± 3 (GI) and 4 ± 1 minutes (GII). No statistical differences were found in analyses, although time to intubation was less in GII. The results suggested that both combinations could be used safely for anesthetic induction in healthy dogs.     

Post-prandial serum bile acid concentrations and ammonia tolerance in Maltese dogs with and without hepatic vascular anomalies

SUMMARY: Post-prandial serum bile acid concentrations were measured in 200 Maltese dogs in an attempt to identify those with subclinical portosystemic shunts. Five of these were later shown to have hepatic pathology or abnormal liver function. In the other 195 Maltese bile acid concentrations ranged from 1 to 362 μmol.L^-1 (mean ± SD, 70 ±50 μmol.L^-1; median, 65.0 μmol.L^-1). Of these, 79% were above the reference range (0 to 31 μmol.L^-1) established from 23 mixed-breed control dogs. It was therefore not possible to determine the prevalence of subclinical portosystemic shunts on the basis of bile acid determinations.
Further investigation of liver function was performed to investigate why bile acid concentrations were increased in these dogs. Rectal ammonia tolerance tests were normal in 102 of 106 Maltese tested and liver samples (11 dogs) and plasma biochemistry profiles (9 dogs) demonstrated no significant hepatic disease or dysfunction.
Of 2 Maltese with hyperammonaemia after administration of ammonium chloride, one had a large congenital portosystemic shunt that was confirmed at surgery. In the other there were no macroscopic portosystemic communications, but a liver biopsy showed histological changes consistent with microscopic portovascular dysplasia.
Total serum bile acid concentrations were consistently lower when assessed by highperformance liquid chromatography than by an enzymatic spectrophotometric method. This discrepancy was substantially larger in Maltese than in control dogs, suggesting the presence of an additional reacting substance in the serum of Maltese dogs.     

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.     

Respiratory function and extraocular muscle paralysis following administration of pancuronium bromide in dogs

Pancuronium bromide, a neuromuscular blocking agent, was evaluated in canine cataract surgical patients under general anesthesia to determine its effects on respiratory function and globe position. Two paralytic, anesthetic regimes were studied: one using a standard dosage of 0.066 mg kg⁻¹ pancuronium bromide, given intravenously while providing the patient with ventilatory support, and one using a dosage of 0.022 mg kg⁻¹ in which no ventilatory support was provided. Eye position and anterior vitreal position/displacement were recorded by a surgeon who was blinded as to treatment group. Physiological parameters indicative of respiratory function were monitored. Both dosages of pancuronium produced comparable, neutral globe position within 30 s following administration which lasted for 20–30 min. All patients in the standard dose group experienced uneventful anesthetic episodes with physiological parameters well within the normal ranges. Within 5 min after administration, all patients in the low-dose group developed a pronounced respiratory acidosis (mean arterial pH = 7.07 ± 0.08; mean PaCO₂ = 79.8 ± 10.7 mmHg), which exceeded a set of predetermined safety limits, and subsequently these dogs received ventilatory support. We conclude that 0.022 mg kg⁻¹ pancuronium rapidly produces an unacceptable level of respiratory acidosis and, as a result, patients receiving neuromuscular blocking agents should routinely receive ventilatory support.     

Efficacy of 1.25% amitraz solution in the treatment of generalized demodicosis (eight cases) and sarcoptic mange (five cases) in dogs

Eight dogs with generalized demodicosis and five with sarcoptic mange were treated with 1.25% amitraz solution applied weekly and associated with an antidote treatment (atipamezol, 0.1 mg kg⁻¹ IM once: and yohimbine 0.1 mg kg⁻¹ once daily for 3 days, orally). Results of skin scrapings were used to determine whether therapy should be continued or stopped. The median number of treatments for demodicosis and sarcoptic mange was three (range 2–5) and two (range 1–3), respectively. Some side-effects were observed but all were stopped with antidote treatment; no failure or relapses occurred at 6–36 months after treatment.     

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.     

ABCB1-1Δ (MDR1-1Δ) genotype is associated with adverse reactions in dogs treated with milbemycin oxime for generalized demodicosis

Twenty-two dogs diagnosed with generalized demodicosis were treated with milbemycin oxime (MO) because of poor response to previous therapies or because the dog was a breed known to be susceptible to ivermectin toxicosis. Fifteen of the 22 dogs were herding breeds. Doses of MO ranged from 1.0 to 2.2 mg kg⁻¹ day⁻¹ per os. Cheek swab samples were obtained in order to determine each dog's ABCB 1 genotype. Adverse drug reactions were recorded for each dog by the owners and/or veterinarians. The ABCB 1-1Δ genotype was significantly associated with the development of an adverse reaction (neurological toxicity) after treatment with MO. None of the 19 dogs with the wild-type ABCB1 allele experienced adverse reactions, whereas two dogs homozygous for the ABCB1-1Δ mutation developed ataxia. Assessing the ABCB1-1Δ genotype prior to MO administration may prevent neurological toxicity in these patients.