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

OBJECTIVE: To evaluate the effects of ketamine, diazepam, and the combination of ketamine and diazepam on intraocular pressures (IOPs) in clinically normal dogs in which premedication was not administered. ANIMALS: 50 dogs. PROCEDURES: Dogs were randomly allocated to 1 of 5 groups. Dogs received ketamine alone (5 mg/kg [KET5] or 10 mg/kg [KET10], IV), ketamine (10 mg/kg) with diazepam (0.5 mg/kg, IV; KETVAL), diazepam alone (0.5 mg/kg, IV; VAL), or saline (0.9% NaCl) solution (0.1 mL/kg, IV; SAL). Intraocular pressures were measured immediately before and after injection and at 5, 10, 15, and 20 minutes after injection. RESULTS: IOP was increased over baseline values immediately after injection and at 5 and 10 minutes in the KET5 group and immediately after injection in the KETVAL group. Compared with the SAL group, the mean change in IOP was greater immediately after injection and at 5 and 10 minutes in the KET5 group. The mean IOP increased to 5.7, 3.2, 3.1, 0.8, and 0.8 mm Hg over mean baseline values in the KET5, KET10, KETVAL, SAL, and VAL groups, respectively. All dogs in the KET5 and most dogs in the KETVAL and KET10 groups had an overall increase in IOP over baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with baseline values and values obtained from dogs in the SAL group, ketamine administered at a dose of 5 mg/kg, IV, caused a significant and clinically important increase in IOP in dogs in which premedication was not administered. Ketamine should not be used in dogs with corneal trauma or glaucoma or in those undergoing intraocular surgery.     

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.     

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.     

The effects of ketamine hydrochloride and diazepam on the intraocular pressure and pupil diameter of the dog’s eye

Objective To determine the effects of 10% ketamine hydrochloride and 0.5% diazepam on intraocular pressure (IOP) and horizontal pupil diameter (HPD) in the canine eye. Procedures Ten healthy dogs for each treatment group were used in this study. In the first group, 20 mg/kg ketamine hydrochloride was injected intravenously; in the second, 0.5 mg/kg diazepam was similarly injected; and in the third, a control group, 0.9% saline was used. In all groups, IOP and HPD were measured every 5 min for 35 min in the first group, and 60 min in the second and third group. Results A maximum increase in IOP was obtained 5 min after ketamine injection, with IOP of 23.2 ± 5.8 mmHg (a 45.0% increase compared to baseline) in the right eye and 22.9 ± 5.9 mmHg (a 43.5% increase) in the left eye (both significant at P < 0.01). A significant IOP increase was observed throughout the research period of 35 min. Statistically significant increases in HPD (P < 0.05) were observed only at 5 and 25 min after ketamine injection. A significant increase in IOP was obtained 10 min after diazepam injection, showing a maximum IOP 20 ± 5.0 mmHg in the right eye (9.3% increase) and 19.9 ± 5.1 mmHg (8.7% increase) in the left eye (both significant at P < 0.05). HPD decreased during the study period, reaching the lowest level 30 min post‐treatment. Conclusions This study showed a substantial increase in IOP after ketamine injection and a less substantial, but still significant increase after diazepam injection. These findings should be taken into consideration when using these drugs in dogs with fragile corneas, or in dogs predisposed or affected by glaucoma.     

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.     

The effects of ketamine‐midazolam anesthesia on intraocular pressure in clinically normal dogs

Objective To determine the effects of intravenous ketamine‐midazolam anesthesia on intraocular pressure (IOP) in ocular normotensive dogs. Animals Thirteen adult mixed‐breed dogs. Procedures Dogs were randomly assigned to treatment (n = 7) and control (n = 6) groups. Dogs in the treatment group received intravenous ketamine 15 mg/kg and midazolam 0.2 mg/kg and dogs in the control group received intravenous saline. The time of intravenous drug injection was recorded (T₀). Measurements of IOP were then repeated 5 min (T₅) and 20 min (T₂₀) following the intravenous administration of ketamine‐midazolam combination and saline in both groups. Results Measurements showed normal IOP values in both groups. The mean ± SD baseline IOP values for treatment and control groups were 13.00 ± 1.47 and 10.33 ± 2.20, respectively. For baseline IOP values, there was no significant difference between treatment and control groups (P = 0.162). In the treatment group, the subsequent post‐treatment mean ± SD values were 15.64 ± 2.17 (5 min), and 14.92 ± 1.98 (20 min). There was no evidence of statistical difference between baseline values and post‐treatment values after treatment with ketamine‐midazolam (P₅ = 0.139; P₂₀ = 0.442). In control eyes, the mean ± SD values at 5 and 20 min were 10.41 ± 2.01 and 10.16 ± 1.69, respectively. There was no significant difference between baseline values and post‐treatment values in control group (P₅ = 1.000; P₂₀ = 1.000). Conclusion Ketamine‐midazolam combination has no clinically significant effect on IOP in the dog.     

Effects of metaraminol bitartrate on intraocular pressure in dogs under halothane anesthesia

The effects of metaraminol bitartrate on intraocular pressure (IOP) were studied in dogs anesthetized with halothane. Forty-five healthy, adult, mixed-breed dogs, of both sexes, were divided into three groups of 15 dogs each (GI, GII and GIII) and maintained under general anesthesia with halothane after tranquilization with levomepromazine and induction with thiopental. Saline (0.9%) was administered intravenously (IV) to GI through continuous infusion, at a velocity of 0.125 mL kg⁻¹ min⁻¹. GII and GIII received metaraminol 0.004% IV, at a dose of 5 μg kg⁻¹ min⁻¹, at 0.125 mL kg⁻¹ min⁻¹ and at a dose of 2 μg kg⁻¹ min⁻¹, at 0.06 mL kg⁻¹ min⁻¹, respectively. IOP was measured by applanation tonometry (Tono-Pen) before and during anesthesia. Results showed that IOP decreased in GI, increased in GII, and remained at basal levels in GIII. Continuous infusion of metaraminol at 2 μg kg min⁻¹ maintained IOP at pretest levels, while infusion at 5 μg kg⁻¹ min⁻¹ produced an elevation of IOP.     

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.     

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.     

Alfaxalone in cyclodextrin for induction and maintenance of anaesthesia in ponies undergoing field castration

Objective  To evaluate the induction and maintenance of anaesthesia using alfaxalone following pre-anaesthetic medication with romifidine and butorphanol in ponies undergoing castration in the field.
Study design  Prospective clinical study.
Animals  Seventeen male ponies weighing 169 ± 29 kg.
Methods  The ponies were sedated with romifidine and butorphanol intravenously (IV). Induction time was recorded following administration of alfaxalone 1 mg kg⁻¹ and diazepam 0.02 mg kg⁻¹ IV. If movement during surgery occurred, alfaxalone 0.2 mg kg⁻¹ was administered IV. The quality of anaesthetic induction, and recovery were scored on a subjective scale of 1 (good) to 5 (poor). The number of attempts to attain sternal recumbency and standing, quality of recovery and times from induction to end of surgery, first head lift, sternal recumbency and standing were recorded.
Results  Induction quality was good [median score (range) 1 (1–3)] with a mean ± SD time of 29 ± 6 seconds taken to achieve lateral recumbency. Ten ponies required incremental doses of alfaxalone during surgery. Mean times to the end of surgery, first head lift, sternal recumbency and standing were 26 ± 9 minutes, 31 ± 9 minutes, 33 ± 9 minutes and 34 ± 9 minutes respectively. The number of attempts to attain sternal recumbency was 1(1–1) and to attain standing was 1(1–2). Quality of recovery was good, with a recovery score of 1(1–2).
Conclusions and clinical relevance  Alfaxalone provided smooth induction and recovery characteristics and was considered suitable for maintenance of anaesthesia for castration in ponies.     

Clinical and immunomodulating effects of ketamine in horses with experimental endotoxemia

Background: Ketamine has immunomodulating effects both in vitro and in vivo during experimental endotoxemia in humans, rodents, and dogs. Hypothesis: Subanesthetic doses of ketamine will attenuate the clinical and immunologic responses to experimental endotoxemia in horses. Animals: Nineteen healthy mares of various breeds. Methods: Experimental study. Horses were randomized into 2 groups: ketamine‐treated horses (KET; n = 9) and saline‐treated horses (SAL; n = 10). Both groups received 30 ng/kg of lipopolysaccharide (LPS, Escherichia coli, O55:B5) 1 hour after the start of a continuous rate infusion (CRI) of racemic ketamine (KET) or physiologic saline (SAL). Clinical and hematological responses were documented and plasma concentrations of tumor necrosis factor‐α (TNF‐α) and thromboxane B₂ (TXB₂) were quantified. Results: All horses safely completed the study. The KET group exhibited transient excitation during the ketamine loading infusion (P < .05) and 1 hour after discontinuation of administration (P < .05). Neutrophilic leukocytosis was greater in the KET group 8 and 24 hours after administration of LPS (P < .05). Minor perturbations of plasma biochemistry results were considered clinically insignificant. Plasma TNF‐α and TXB₂ production peaked 1.5 and 1 hours, respectively, after administration of LPS in both groups, but a significant difference between treatment groups was not demonstrated. Conclusions and Clinical Importance: A subanesthetic ketamine CRI is well tolerated by horses. A significant effect on the clinical or immunologic response to LPS administration, as assessed by clinical observation, hematological parameters, and TNF‐α and TXB₂ production, was not identified in healthy horses with the subanesthetic dose of racemic ketamine utilized in this study.     

Use of ketamine, xylazine, and diazepam anesthesia with retrobulbar block for phacoemulsification in dogs

Objective  The study was undertaken to evaluate the use of ketamine, xylazine, and diazepam along with a local retrobulbar nerve block for routine phacoemulsification in the dog.
Animals  Ten clinically healthy mixed-breed dogs of either sex, weighing between 10 and 15 kg.
Procedures  Ten mixed-breed dogs were selected for unilateral cataract removal by phacoemulsification. Standard preoperative preparations for cataract surgery were followed. Pre-anesthetic medication consisted of atropine sulfate (0.02 mg/kg, SC). Anesthesia was induced by xylazine HCl (1.0 mg/kg, IM) followed by ketamine (5.0 mg/kg, IM). Anesthesia was maintained subsequently with IV ketamine and diazepam to effect and depth of anesthesia was assessed clinically by pedal reflex and jaw reflex. After induction of anesthesia, a retrobulbar nerve block was performed using 2 mL of 2% lignocaine. Eye position was graded after retrobulbar block and IOP was examined preoperative, post-anesthetic, 6 h postoperative and 24 h after surgery. Phacoemulsification was performed using the phaco-chop technique and an intraocular lens was placed. Anesthetic recovery and postoperative recovery following surgery was recorded.
Result  The exposure of the globe in all the dogs was adequate; the desired central fixation of the eye was obtained and surgery could be performed uneventfully. The mean IOP recorded after induction of anesthesia was 15.75 ± 0.82, which was not significantly ( P  > 0.01) different from pre-anesthetic values (14.85 ± 0.85).
Conclusion  Phacoemulsification was successfully performed with this anesthetic regimen without encountering major intraoperative or anesthetic complications.     

Effect of metoclopramide on gastro-esophageal reflux in anesthetized dogs

Administration of morphine before anesthesia leads to gastro-esophageal reflux (GER) in over 50% of dogs during the subsequent anesthetic. This GER is clinically silent but can lead to aspiration pneumonitis, esophagitis and esophageal stricture. In this prospective clinical study we aimed to determine the effect of metoclopramide on gastro-esophageal reflux (GER) in dogs undergoing elective orthopedic surgery. Dogs were admitted to the study if they were healthy, and had no history of vomiting or dysphagia. Dogs were fasted for an average of 18.2 ± 4.3 (mean ± SD) hours prior to induction of anesthesia. Anesthesia in all dogs included acepromazine, morphine, thiopental and isoflurane in oxygen. By random allocation, half the dogs received metoclopramide (M) as an IV bolus (0.4 mg kg^–1) and then infusion (0.3 mg kg^–1hour^–1), the others received equivalent volumes of saline (S). To measure esophageal pH a sensor-tipped catheter was placed with the tip 5–7 cm cranial to the lower esophageal sphincter, and connected to a computer for continual data collection. The pH of any fluid running from the mouth or nose was measured. Gastro-esophageal reflux was defined as a decrease in esophageal pH below 4 or an increase above 7.5. Fisher's Exact test was used to test significance of differences in incidence between groups. Separate multivariable logistic regression models were created for each outcome to assess the effects of risk factors on outcome. There were seven cases of GER in 16 dogs receiving M and 8/14 in those receiving S. There were no significant differences between M and S treated dogs in age, weight, duration of anesthesia and fasting, thiopental dose or incidence of vomiting. The administration of metoclopramide at this dose did not significantly reduce the incidence of GER in these anesthetized dogs.     

Effect of pre-anesthetic meperidine on gastro-esophageal reflux in anesthetized dogs

Meperidine has been shown to decrease lower esophageal sphincter tone in monkeys and people, to have little effect in cats, and to physically increase it in dogs. We hypothesized that administration of meperidine to dogs before anesthesia would decrease the probability of GER during the subsequent anesthetic. In this randomized, prospective clinical trial we aimed to determine the incidence of GER in dogs undergoing elective orthopedic surgery and receiving either meperidine or morphine prior to anesthesia. Dogs were admitted to the study, if they were healthy, with no history of vomiting or dysphagia. Dogs were fasted overnight. Dogs were received either morphine (0.66 mg kg^–1 IM) or meperidine (8.8 mg kg^–1 IM) with acepromazine. Anesthesia in all dogs included thiopental and isoflurane in oxygen. To measure esophageal pH a sensor-tipped catheter was placed with the tip 5–7 cm cranial to the lower esophageal sphincter, and connected to a computer for continual data collection. Dogs were observed for vomiting after pre-medication, and the pH of any fluid running from the mouth or nose during anesthesia was measured. Gastro-esophageal reflux was defined as a decrease in esophageal pH below 4 or an increase above 7.5 for greater than 15 seconds. One-way anova was used to test significance of differences between groups in parametric variables. Fisher's Exact test was used to test significance of differences in incidence between groups. In dogs receiving meperidine the incidence of vomiting was 0, and of GER was 31% (4/13), compared to 60% (6/10) and 60% (6/10), respectively in dogs receiving morphine. In this preliminary study, the administration of pre-anesthetic meperidine was associated with a 29% reduction in the absolute risk of GER compared to morphine.     

Plasma and ear tissue concentrations of enrofloxacin and its metabolite ciprofloxacin in dogs with chronic end-stage otitis externa after intravenous administration of enrofloxacin

The purpose of this study was to measure the concentrations of enrofloxacin and its metabolite ciprofloxacin following intravenous administration of enrofloxacin in the plasma and ear tissue of dogs with chronic end-stage otitis undergoing a total ear canal ablation and lateral bulla osteotomy. The goals were to determine the relationship between the dose of enrofloxacin and the concentrations of enrofloxacin and ciprofloxacin, and determine appropriate doses of enrofloxacin for treatment of chronic otitis externa and media. Thirty dogs were randomized to an enrofloxacin-treatment group (5, 10, 15 or 20 mg kg⁻¹) or control group (no enrofloxacin). After surgical removal, ear tissue samples (skin, vertical ear canal, horizontal ear canal, middle ear) and a blood sample were collected. Concentrations of enrofloxacin and ciprofloxacin in the plasma and ear tissue were measured by high performance liquid chromatography. Repeated measures models were applied to log-transformed data to assess dosing trends and Pearson correlations were calculated to assess concentration associations. Ear tissue concentrations of enrofloxacin and ciprofloxacin were significantly ( P  < 0.05) higher than plasma concentrations. Each 5 mg kg⁻¹ increase in the dose of enrofloxacin resulted in a 72% and 37% increase in enrofloxacin and ciprofloxacin concentrations, respectively. For bacteria with an minimal inhibitory concentration of 0.12–0.15 or less, 0.19–0.24, 0.31–0.39 and 0.51–0.64 µg mL⁻¹, enrofloxacin should be dosed at 5, 10, 15 and 20 mg kg⁻¹, respectively. Treatment with enrofloxacin would not be recommended for a bacterial organism intermediate or resistant in susceptibility to enrofloxacin since appropriate levels of enrofloxacin would not be attained.     

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.

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.     

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.     

Analgesic and motor-blocking action of epidurally administered levobupivacaine or bupivacaine in the conscious dog

Objective  To compare the analgesic and motor-blocking effects of epidurally administered levobupivacaine and bupivacaine in the conscious dog.
Study design  Prospective, randomized, cross-over study.
Animals  Six adult female Beagle dogs.
Methods  Each animal received three doses of levobupivacaine or bupivacaine (0.5, 1.0 and 1.5 mg kg⁻¹; concentrations 0.25%, 0.50%, and 0.75%, respectively) in a total volume of 0.2 mL kg⁻¹ by means of a chronically implanted epidural catheter. Onset, duration (through pinch response in the sacral, lumbar and toe areas) and degree of analgesia and motor-blocking status was determined with a scoring system and at regular intervals over 8.5 hours before (baseline) and after drug administration.
Results  Epidurally administered levobupivacaine and bupivacaine had a similar dose-dependent analgesic action with no significant differences in onset (range: 5–8 minutes), duration (bupivacaine: 42 ± 28, 135 ± 68 and 265 ± 68 minutes, and levobupivacaine: 28 ± 33, 79 ± 55 and 292 ± 133 minutes; 0.25%, 0.50%, and 0.75%, respectively) or maximum degree of analgesia. However, levobupivacaine tended to produce a shorter duration of motor block than bupivacaine and the difference in the motor to nociceptive blockade times was significant at the highest dose.
Conclusion  Epidural levobupivacaine produced an analgesic action similar to that of bupivacaine.
Clinical relevance  Epidural levobupivacaine is suitable for clinical use in dogs, mostly at the highest dose if a high degree of analgesia is required.     

Transient unilateral Horner's syndrome after epidural ropivacaine in a dog

Observations  A left sided Horner's syndrome (ptosis, prolapse of the nictitating membrane and miosis) was observed in a 4-year-old female, neutered Beagle dog after epidural injection of 0.22 mL kg⁻¹ ropivacaine (0.75%) in 0.01 mL kg⁻¹ of saline during isoflurane anaesthesia. Clinical signs disappeared gradually and resolved completely 4 hours and 10 minutes after injection.
Conclusions  The epidural injection of 0.22 mL kg⁻¹ ropivacaine (0.75%) in 0.01 mL kg⁻¹ of saline during isoflurane anaesthesia caused unilateral (left) Horner's syndrome in a 4-year-old female, neutered Beagle dog.