Effects of levomepromazine and different desflurane concentrations upon electrocardiographic variables in dogs

Objectives To investigate the effects of levomepromazine and different desflurane concentrations upon electrocardiographic variables. Animals Twenty adult mongrel dogs of both sexes weighing 6–28 kg. Methods Dogs were divided into two groups of 10 animals. Group 1 received 1 mg kg^?1 IV of levomepromazine and 15 minutes later anesthesia was induced with propofol (3 mg kg^?1 IV). Desflurane end‐tidal concentration was set at 1.6 MAC. After 30 minutes at this concentration, measurements were taken and the end‐tidal concentration was reduced to 1.4 MAC. Thereafter, it was reduced to 1.2 and then 1.0 MAC at 15‐minute intervals. The same procedure was followed for group 2, except that levomepromazine was replaced with 0.2 mL kg^?1 of 0.9% saline solution and more propofol was needed for induction (7 mg kg^?1). The animals' body temperature was maintained between 38.3 and 39 °C using a heating pad. The electrocardiographic tracing was obtained from lead II throughout the experimental period. The measurements were taken immediately before the administration of levomepromazine or placebo (T₁), 15 minutes after pre‐medication (T₂) and 30 minutes after the establishment of 1.6 MAC (T₃). The other measurements were made at the concentrations of 1.4, 1.2, and 1.0 MAC, respectively (T_4?6). The numerical data were submitted to analysis of variance plus F‐test (p < 0.05). Results The dogs that received levomepromazine had a decrease in heart rate. However, in both groups it increased with desflurane administration. Levomepromazine, in association with desflurane, did not induce significant electrocardiographic changes, and all mean values (except P‐wave duration) were within the reference range for this species. Conclusions and clinical relevance This study documented that levomepromazine, in association with desflurane, does not induce significant changes in electrocardiographic variables, suggesting that this drug combination has minimal effect on myocardial conduction.     

Continuous infusion of ketamine in hypovolemic dogs anesthetized with desflurane

Objective: To evaluate the cardiorespiratory effects of continuous infusion of ketamine in hypovolemic dogs anesthetized with desflurane. Design: A prospective experimental study. Animals: Twelve mixed breed dogs allocated into 2 groups: saline (n=6) and ketamine (n=6). Interventions: After obtaining baseline measurements (time [T] 0) in awake dogs, hypovolemia was induced by the removal of 40 mL of blood/kg over 30 minutes. Anesthesia was induced and maintained with desflurane (1.5 minimal alveolar concentration) and 30 minutes later (T75) a continuous intravenous (IV) infusion of saline or ketamine (100 μg/kg/min) was initiated. Cardiorespiratory evaluations were obtained 15 minutes after hemorrhage (T45), 30 minutes after desflurane anesthesia, and immediately before initiating the infusion (T75), and 5 (T80), 15 (T90), 30 (T105) and 45 (T120) minutes after beginning the infusion. Measurements and main results: Hypovolemia (T45) reduced the arterial blood pressures (systolic arterial pressure, diastolic arterial pressure [DAP] and mean arterial pressure [MAP]), cardiac (CI) and systolic (SI) indexes, and mean pulmonary arterial pressure (PAP) in both groups. After 30 minutes of desflurane anesthesia (T75), an additional decrease of MAP in both groups was observed, heart rate was higher than T0 at T75, T80, T90 and T105 in saline‐treated dogs only, and the CI was higher in the ketamine group than in the saline group at T75. Five minutes after starting the infusion (T80), respiratory rate (RR) was lower and the end‐tidal CO₂ (ETCO₂) was higher compared with values at T45 in ketamine‐treated dogs. Mean values of ETCO₂ were higher in ketamine than in saline dogs between T75 and T120. The systemic vascular resistance index (SVRI) was decreased between T80 and T120 in ketamine when compared with T45. Conclusions: Continuous IV infusion of ketamine in hypovolemic dogs anesthetized with desflurane induced an increase in ETCO₂, but other cardiorespiratory alterations did not differ from those observed when the same concentration of desflurane was used as the sole anesthetic agent. However, this study did not evaluate the effectiveness of ketamine infusion in reducing desflurane dose requirements in hypovolemic dogs or the cardiorespiratory effects of ketamine–desflurane balanced anesthesia.     

Evaluation of intraocular pressure in association with cardiovascular parameters in normocapnic dogs anesthetized with sevoflurane and desflurane

The objective of this study was to determine intraocular pressure (IOP) and cardiac changes in normocapnic dogs maintained under controlled ventilation and anesthetized using sevoflurane or desflurane. Sixteen healthy adult mixed-breed dogs, seven males and nine females, weighing 10-15 kg were used. The dogs were randomly assigned to one of two groups composed of eight animals anesthetized with sevoflurane (SEVO) or desflurane (DESF). In both groups, anesthesia was induced with propofol (10 mg/kg), and neuromuscular blockade was achieved with rocuronium (0.6 mg/kg/h i.v.). No premedication was given. Ventilation was adjusted to maintain end-tidal carbon dioxide partial pressure at 35 mmHg. Anesthesia was maintained with 1.5 minimum alveolar concentration (MAC) of sevoflurane or desflurane. In both groups IOP was measured by applanation tonometry (Tono-Pen) before induction of anesthesia. IOP, mean arterial pressure (MAP), heart rate (HR), cardiac index (CI) and central venous pressure (CVP) were also measured 45 min after the beginning of inhalant anesthesia and then every 20 min for 60 min. A one-way repeated measures anova was used to compare data within the same group and Student's t-test was used to assess differences between groups. P < 0.05 was considered statistically significant. Measurements showed normal IOP values in both groups, even though IOP increased significantly from baseline during the use of desflurane. IOP did not differ between groups. CI in the desflurane group was significantly greater than in the sevoflurane group. Sevoflurane and desflurane have no clinically significant effects on IOP, MAP, HR, CI or VCP in the dog.     

Effects of nitrous oxide on IOP and pupillary diameter in dogs anesthetized with varying concentrations of desflurane

Objective The aim of the present study was to evaluate the effects of nitrous oxide on IOP and pupillary diameter (PD) of dogs anesthetized with varying desflurane concentrations. Animals studied Twenty adult Mongrel dogs were used. Methods They were anesthetized with propofol (10 mg/kg, IV) and maintained with varying concentrations of desflurane (1.6, 1.4, and 1.2 MAC) diluted in 100% oxygen (G1) or in 70% nitrous oxide and 30% oxygen (G2) (30 mL/kg/min). IOP was measured by applanation tonometry and horizontal PD was taken with a caliper adjacent to the cornea. Mean arterial pressure (MAP), heart rate (HR), respiratory rate (RR), and end‐tidal CO₂ (etCO₂) were also measured. All parameters were measured at T0, T30, T45, and T60 time points. One‐way repeated measures anova and the t‐test were used to assess statistical differences (P < 0.05). Results T30, T45, and T60 IOP measures were within normal limits for both groups and IOP did not differ between groups at any time. There was a significant decrease in PD in G1 between T0 and T30, T45 and T60, and also between T30 and T60. PD did not differ between groups. All vital parameters were within normal limits throughout anesthesia. Conclusions Administration of nitrous oxide with desflurane results in maintenance of normal IOP and prevents a decrease in horizontal PD during anesthesia. Therefore, this may be a suitable protocol in dogs undergoing intraocular surgeries that require mydriasis and maintenance of normal IOP.     

Minimum alveolar concentration of desflurane in llamas and alpacas

OBJECTIVE: To determine the minimum alveolar concentration (MAC) of desflurane in llamas and alpacas. DESIGN: Prospective study. Animals Six healthy adult llamas and six healthy adult alpacas. PROCEDURE: Anesthesia was induced with desflurane delivered with oxygen through a mask. An endotracheal tube was inserted, and a port for continuous measurement of end-tidal and inspired desflurane concentrations was placed between the endotracheal tube and the breathing circuit. After equilibration at an end-tidal-to-inspired desflurane concentration ratio >0.90 for 15 minutes, a 50-Hz, 80-mA electrical stimulus was applied to the antebrachium until a response was obtained (i.e. gross purposeful movement) or for up to 1 minute. The vaporizer setting was increased or decreased to effect a 10-20% change in end-tidal desflurane concentration, and equilibration and stimulus were repeated. The MAC was defined as the average of the lowest end-tidal desflurane concentration that prevented a positive response and the highest concentration that allowed a positive response. RESULTS: Mean +/- SD MAC of desflurane was 7.99 +/- 0.58% in llamas and 7.83 +/- 0.51% in alpacas. CONCLUSIONS AND CLINICAL RELEVANCE: The MAC of desflurane in llamas and alpacas was in the range of that reported for other species.     

Cardiopulmonary effects of desflurane in horses

OBJECTIVE: To determine the cardiopulmonary effects of desflurane (DES) in horses. ANIMALS: Six healthy adult horses, three males and three females, aged 9 +/- 4 (mean +/- SD) years and weighing 370 +/- 36 kg. MATERIALS AND METHODS: Anaesthesia was induced with an O2 (10 L minute(-1)) and DES mixture (vaporizer setting 18%). After oro-tracheal intubation, horses were positioned in right lateral recumbency. Anaesthesia was maintained with DES in O2 (20 mL kg(-1) minute(-1)) delivered through a large animal circle breathing system. The minimum alveolar concentration of DES (MAC(DES)) that prevented purposeful movement in response to 60 seconds of electrical stimulation of the oral mucous membranes was determined for each horse. The delivered concentration of DES was then increased to achieve end-tidal concentrations corresponding to 1.5 x MAC(DES), 1.75 x MAC(DES), and 2.0 x MAC(DES). Heart rate (HR), mean arterial blood pressure (MAP), respiratory rate (fr), tidal volume (VT), minute volume (VM) and core temperature were determined, and blood samples for arterial blood gas analysis taken at each DES concentration. All data were analysed by two-way anova for repeated measures and Fisher's test for multiple comparisons. A probability level of p < 0.05 was applied. RESULTS: Desflurane concentrations of 2.0 x MAC(DES) increased HR whereas lower concentrations did not. Mean arterial pressure was not affected by 1.0 x MAC(DES) 1.5 x MAC(DES) or 1.75 x MAC(DES), whereas it decreased at 2.0 x MAC(DES). All concentrations of DES examined significantly depressed fr, VT and VM. CONCLUSIONS AND CLINICAL RELEVANCE: Desflurane concentrations between 1.0 and 1.75 x MAC(DES) reduces fr and VM but does not affect HR or MAP in horses.     

Cardiovascular and respiratory effects of two doses of fentanyl in the presence or absence of bradycardia in isoflurane-anesthetized dogs

Objective

To compare the cardiopulmonary effects of low and high doses of fentanyl before and after the correction of bradycardia in isoflurane-anesthetized dogs.

Cardiovascular effects following epidural injection of romifidine in isoflurane‐anaesthetized dogs

ObjectiveTo investigate the cardiovascular effects of epidural romifidine in isoflurane-anaesthetized dogs.Study designProspective, randomized, blinded experiment.AnimalsA total of six healthy adult female Beagles aged 1.25 ± 0.08 years and weighing 12.46 ± 1.48 (10.25–14.50) kg.MethodsAnaesthesia was induced with propofol (6–9 mg kg^?1) and maintained with 1.8–1.9% end-tidal isoflurane in oxygen. End-tidal CO₂ was kept between 35 and 45 mmHg (4.7–6.0 kPa) using intermittent positive pressure ventilation. Heart rate (HR), arterial blood pressure and cardiac output (CO) were monitored. Cardiac output was determined using a LiDCO monitor and the derived parameters were calculated. After baseline measurements, either 10 μg kg^?1 romifidine or saline (total volume 1 mL 4.5 kg^?1) was injected into the lumbosacral epidural space. Data were recorded for 1 hour after epidural injection. A minimum of 1 week elapsed between treatments.ResultsAfter epidural injection, the overall means (± standard deviation, SD) of HR (95 ± 20 bpm), mean arterial blood pressure (MAP) (81 ± 19 mmHg), CO (1.63 ± 0.66 L minute^?1), cardiac index (CI) (2.97 ± 1.1 L minute^?1 m^?2) and stroke volume index (SI) (1.38 ± 0.21 mL beat^?1 kg^?1) were significantly lower in the romifidine treatment compared with the overall means in the saline treatment [HR (129 ± 24 bpm), MAP (89 ± 17 mmHg), CO (3.35 ± 0.86 L minute^?1), CI (6.17 ± 1.4 L minute^?1 m^?2) and SI (2.21 ± 0.21 mL beat^?1 kg^?1)]. The overall mean of systemic vascular resistance index (SVRI) (7202 ± 2656 dynes seconds cm^?5 m^?2) after epidural romifidine injection was significantly higher than the overall mean of SVRI (3315 ± 1167 dynes seconds cm^?5 m^?2) after epidural saline injection.ConclusionEpidural romifidine in isoflurane-anaesthetized dogs caused significant cardiovascular effects similar to those reportedly produced by systemic romifidine administration.Clinical relevanceSimilar cardiovascular monitoring is required after epidural and systemically administered romifidine. Further studies are required to evaluate the analgesic effects of epidural romifidine.     

Cardiovascular effects of sevoflurane in Holstein calves

Objective The purpose of this study was to determine the cardiovascular effects of sevoflurane in calves. Study design Prospective experimental study. Animals Six, healthy, 8–12‐week‐old Holstein calves weighing 80 ± 4.5 (mean ± SEM) kg were studied. Methods Anesthesia was induced by face‐mask administration of 7% sevoflurane in O₂. Calves tracheae were intubated, placed in right lateral recumbency, and maintained with 3.7% end‐tidal concentration sevoflurane for 30 minutes to allow catheterization of the auricular artery and placement of a Swan‐Ganz thermodilution catheter into the pulmonary artery. After instrumentation, administration of sevoflurane was temporarily discontinued until mean arterial pressure was > 100 mm Hg. Baseline values were recorded and the vaporizer output increased to administer 3.7% end‐tidal sevoflurane concentration. Ventilation was controlled to maintain normocapnia. The following were recorded at 5, 10, 15, 30 and 45 minutes after collection of baseline data and expressed as the mean value (± SEM): direct systolic, diastolic, and mean arterial blood pressures; cardiac output; mean pulmonary arterial pressure; pulmonary arterial occlusion pressure, heart rate; and pulmonary arterial temperature. Cardiac index and systemic and pulmonary vascular resistance values were calculated using standard formulae. Arterial blood gases were analyzed at baseline, and at 15 and 45 minutes. Differences from baseline values were determined using one‐way analysis of variance for repeated measures with post‐hoc differences between mean values identified using Dunnet's test (p < 0.05). Results Mean time from beginning sevoflurane administration to intubation of the trachea was 224 ± 9 seconds. The mean end‐tidal sevoflurane concentration at baseline was 0.7 (± 0.11)%. Sevoflurane anesthesia was associated with decreased arterial blood pressure at all sampling times. Mean arterial blood pressure decreased from a baseline value of 112 ± 7 mm Hg to a minimum value of 88 ± 4 mm Hg at 5 minutes. Compared with baseline, arterial pH was decreased at 15 minutes. Pulmonary arterial blood temperature was decreased at 15, 30 and 45 minutes. Arterial CO₂ tension increased from a baseline value of 43 ± 3 to 54 ± 4 mm Hg (5.7 ± 0.4 to 7.2 ± 0.3 kPa) at 15 minutes. Mean pulmonary arterial pressure was increased at 30 and 45 minutes. Pulmonary arterial occlusion pressure increased from a baseline value of 18 ± 2 to 23 ± 2 mm Hg at 45 minutes. There were no significant changes in other measured variables. All calves recovered from anesthesia uneventfully. Conclusion We conclude that sevoflurane for induction and maintenance of anesthesia was effective and reliable in these calves and that neither hypotension nor decreased cardiac output was a clinical concern. Clinical relevance Use of sevoflurane for mask induction and maintenance of anesthesia in young calves is a suitable alternative to injectable and other inhalant anesthetics.     

Hemodynamic effects of incremental doses of acepromazine in isoflurane-anesthetized dogs

ObjectiveTo evaluate the effects of incremental doses of acepromazine on hemodynamics in isoflurane-anesthetized dogs.Study designProspective, experimental study.AnimalsHealthy, adult, mixed-breed dogs (two male and four female) weighing 16.8 ± 5.1 kg (mean ± standard deviation).MethodsDogs were anesthetized with propofol (7 mg kg^–1) intravenously (IV) and isoflurane. Thermodilution and arterial catheters were placed for hemodynamic monitoring and arterial blood sampling for blood gas analysis. Baseline measurements were performed with stable expired concentration of isoflurane (Fe′Iso) at 1.8%. Each dog was then administered four incremental acepromazine injections (10, 15, 25 and 50 μg kg^–1) IV, and measurements were repeated 20 minutes after each acepromazine injection with Fe′Iso decreased to 1.2%. The four acepromazine injections resulted in cumulative doses of 10, 25, 50 and 100 μg kg^–1 (time points ACP₁₀, ACP₂₅, ACP₅₀ and ACP₁₀₀, respectively).ResultsCompared with baseline, cardiac index (CI) increased significantly by 34%, whereas systemic vascular resistance index (SVRI) decreased by 25% at ACP₅₀ and ACP₁₀₀. Arterial oxygen content (CaO₂) was significantly lower than baseline after all acepromazine injections (maximum decreases of 11%) and was lower at ACP₅₀ and ACP₁₀₀ than at ACP₁₀. No significant change was found in heart rate, stroke index, oxygen delivery index and systolic, mean and diastolic blood pressures. Hypotension (mean arterial pressure < 60 mmHg) was observed in one dog at baseline, ACP₁₀, ACP₂₅ and ACP₁₀₀, and in two dogs at ACP₅₀.Conclusions and clinical relevanceCompared with isoflurane alone, anesthesia with acepromazine–isoflurane resulted in increased CI and decreased SVRI and CaO₂ values. These effects were dose-related, being more pronounced at ACP₅₀ and ACP₁₀₀. Under the conditions of this study, acepromazine administration did not change blood pressure.     

Cardiovascular effects of vasopressors in isoflurane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increased to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of vasopressors in halothane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP, with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR.     

Cardiovascular effects of desflurane in mechanically ventilated calves

OBJECTIVE: To determine cardiovascular effects of desflurane in mechanically ventilated calves. ANIMALS: 8 healthy male calves. PROCEDURE: Calves were anesthetized by face mask administration of desflurane to permit instrumentation. Administration of desflurane was temporarily discontinued until mean arterial blood pressure increased to >or= 100 mm Hg, at which time baseline cardiovascular values, pulmonary arterial temperature, end-tidal CO(2) tension, and end-tidal desflurane concentration were recorded. Cardiac index and systemic and pulmonary vascular resistances were calculated. Arterial blood gas variables were measured and calculated. Mean end-tidal concentration of desflurane at this time was 3.4%. After collection of baseline values, administration of 10% end-tidal concentration of desflurane was resumed and calves were connected to a mechanical ventilator. Cardiovascular data were collected at 5, 10, 15, 30, and 45 minutes, whereas arterial blood gas data were collected at 15 and 45 minutes after collection of baseline data. RESULTS: Mean +/- SD duration from beginning desflurane administration to intubation of the trachea was 151 +/- 32.8 seconds. Relative to baseline, desflurane anesthesia was associated with a maximal decrease in arterial blood pressure of 35% and a decrease in systemic vascular resistance of 34%. Pulmonary arterial blood temperature was decreased from 15 through 45 minutes, compared with baseline values. There were no significant changes in other measured variables. All calves recovered from anesthesia without complications. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of desflurane for induction and maintenance of general anesthesia in calves was smooth, safe, and effective. Cardiopulmonary variables remained in reference ranges throughout the study period.     

Cardiovascular effects of dose escalating of norepinephrine in healthy dogs anesthetized with isoflurane

ObjectiveTo evaluate the systemic cardiovascular effects of dose escalating administration of norepinephrine in healthy dogs anesthetized with isoflurane.Study designExperimental study.AnimalsA total of six adult laboratory Beagle dogs, 10.5 (9.2–12.0) kg [median (range)].MethodsEach dog was anesthetized with isoflurane at an end-tidal concentration of 1.7%, mechanically ventilated and administered a continuous rate infusion of rocuronium (0.5 mg kg^–1 hour^–1). Each dog was administered incremental dose rates of norepinephrine (0.05, 0.125, 0.25, 0.5, 1.0 and 2.0 μg kg^–1 minute^–1), and each dose was infused for 15 minutes. Cardiovascular variables were recorded before administration and at the end of each infusion period.ResultsNorepinephrine infusion increased mean arterial pressure (MAP), cardiac output (CO) and oxygen delivery in a dose-dependent manner. Systemic vascular resistance did not significantly change during the experiment. Stroke volume increased at the lower dose rates and heart rate increased at the higher dose rates. Oxygen consumption and lactate concentrations did not significantly change during infusions.ConclusionsIn dogs anesthetized with isoflurane, norepinephrine increased MAP by increasing the CO. CO increased with a change in stroke volume at lower dose rates of norepinephrine. At higher dosage, heart rate also contributed to an increase in CO. Norepinephrine did not cause excessive vasoconstriction that interfered with the CO during this study.Clinical relevanceNorepinephrine can be useful for treating hypotension in dogs anesthetized with isoflurane.     

A review of ophthalmic local and regional anesthesia in dogs and cats

Objective

Orbital and globe surgeries are commonly performed in companion animals and are considered to cause moderate to severe pain. Regional anesthesia techniques can provide complete sensory blockade, analgesia for painful procedures and improve surgical conditions. The purpose of this review is to summarize local and regional anesthesia techniques for ophthalmic surgery in dogs and cats with emphasis on veterinary publications in the past 12 years.

Functional MRI as a tool to assess vision in dogs: the optimal anesthetic

Functional magnetic resonance imaging (fMRI) is a recent advance in neuroimaging that provides a picture of brain activity with excellent spatial resolution. Current methods used to evaluate canine vision are poorly standardized and vulnerable to bias. Functional MRI may represent a valuable method of testing vision in dogs if the impacts of anesthesia on fMRI are understood. Six dogs were scanned during visual stimulation, each under three different anesthetic protocols (isoflurane, propofol, fentanyl/midazolam) to address the questions: (1) Can visually evoked fMR signals be reliably recorded in anesthetized dogs? and (2) Which anesthetic agent permits the least suppression of visually induced fMR signal in dogs? This study confirms that visual stimuli reliably elicit neural activity and fMR signal change in anesthetized dogs. No significant differences in images acquired under the three anesthetics were found, and there was no significant relationship between anesthetic dose and brain activity, within the range of doses used in this study. Images obtained during isoflurane anesthesia were more consistent between dogs than those obtained with the other two agents. This reduced variation may reflect the fact that inhalant anesthesia is more easily controlled than intravenous anesthesia under conditions associated with high field fMRI.