Determination of the minimum alveolar concentration of isoflurane in llamas

OBJECTIVE: To determine the minimum alveolar concentration (MAC) of isoflurane (ISO) in llamas. STUDY DESIGN: Prospective study. ANIMALS: Eight adult neutered male llamas (9 +/- 1 years [x +/- SD], 177 +/- 29 kg). METHODS: Anesthesia was induced and maintained in otherwise unmedicated llamas with a mixture of ISO in oxygen administered through a standard small-animal, semi-closed circle system using an out-of-circle, agent-specific vaporizer. The time from mask placement to intubation was recorded. Inspired and end-tidal (ET) ISO was sampled continuously. At each anesthetic concentration, a constant ET ISO was maintained for at least 20 minutes before application of a noxious electrical stimulus (50 volts, 5 Hz, 10 ms for up to 1 minute). A positive or negative response to the stimulus was recorded, and ET ISO then increased (if positive response) or decreased (if negative response) by 10% to 20%. Individual MAC was the average of multiple determinations. Body temperature was maintained at 37 +/- 1 degrees C. Selected cardiopulmonary variables (heart rate [HR], respiratory rate [RR], arterial blood pressure [ABP]) and ET ISO were recorded at hourly intervals from first ISO. Arterial blood was collected for pH, PCO2, PO2 analysis and measurement of packed cell volume (PCV) and total protein (TP) at 2 hour intervals. Following MAC determination, the anesthetic was discontinued and llamas were allowed to recover. Duration and quality of recovery were noted. RESULTS: The time from start of induction by mask to completion of intubation took 19.1 +/- 4.8 minutes. The MAC of ISO corrected to one atmosphere at sea level (barometric pressure 760 mm Hg) in these llamas was 1.05 +/- 0.17%. Mean ABP increased from 70 +/- 26 mm Hg at the end of the first hour of anesthesia to 102 +/- 7 mm Hg measured at the end of the sixth hour of anesthesia. ET ISO decreased from 2.06 +/- 0.10% to 1.27 +/- 0.07% over the same time period, but MAC did not change with time. The duration from first ISO to discontinuation of ISO averaged 6.19 +/- 0.9 hours. Animals were able to support their heads in a sternal posture at 23 +/- 10 minutes, and stood 62 +/- 26 minutes following discontinuation of the anesthetic. CONCLUSION: The MAC for ISO is similar to, but slightly lower than, values reported for other species. CLINICAL RELEVANCE: Knowledge of MAC may facilitate appropriate clinical use and provide the basis for future investigation of ISO in llamas.     

Comparisons of the effects of acupuncture, electroacupuncture, and transcutaneous cranial electrical stimulation on the minimum alveolar concentration of isoflurane in dogs

OBJECTIVE: To compare the effects of acupuncture (AP), electroacupuncture (EA), and transcutaneous cranial electrical stimulation (TCES) with high-frequency intermittent currents on the minimum alveolar concentration (MAC) of isoflurane and associated cardiovascular variables in dogs. ANIMALS: 8 healthy adult female Beagles. PROCEDURE: Each dog was anesthetized with isoflurane on 4 occasions, allowing a minimum of 10 days between experiments. Isoflurane MAC values were determined for each dog without treatment (controls) and after treatment with AP and EA (AP points included the Large Intestine 4, Lung 7, Governing Vessel 20, Governing Vessel 14, San Tai, and Baihui) and TCES. Isoflurane MAC values were determined by use of noxious electrical buccal stimulation. Heart rate, mean arterial blood pressure (MAP), arterial blood oxygen saturation (Spo2) measured by use of pulse oximetry, esophageal body temperature, inspired and expired end-tidal isoflurane concentrations, end-tidal carbon dioxide concentration, and bispectral index (BIS) were monitored. Blood samples were collected for determination of plasma cortisol concentration. RESULTS: Mean +/- SD baseline MAC of isoflurane was 1.19 +/- 0.1%. Acupuncture did not significantly change MAC of isoflurane. Treatments with EA and TCES significantly lowered the MAC of isoflurane by 10.1% and 13.4%, respectively. The Spo2, heart rate, MAP, BIS, esophageal body temperature, and plasma cortisol concentration were not significantly different after AP, EA, TCES, and control treatments at any time interval. CONCLUSIONS AND CLINICAL RELEVANCE: Use of EA and TCES decreased MAC of isoflurane in dogs without inducing adverse hemodynamic effects. However, the reduction in isoflurane MAC by EA andTCES treatments was not considered clinically relevant.     

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.     

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.     

Minimum alveolar concentration of isoflurane in green iguanas and the effect of butorphanol on minimum alveolar concentration

OBJECTIVE: To determine minimum alveolar concentration (MAC) of isoflurane in green iguanas and effects of butorphanol on MAC. DESIGN: Prospective randomized trial. ANIMALS: 10 healthy mature iguanas. PROCEDURE: in each iguana, MAC was measured 3 times: twice after induction of anesthesia with isoflurane and once after induction of anesthesia with isoflurane and IM administration of butorphanol (1 mg/kg [0.45 mg/lb]). A blood sample was collected from the tail vein for blood-gas analysis at the beginning and end of the anesthetic period. The MAC was determined with a standard bracketing technique; an electrical current was used as the supramaximal stimulus. Animals were artificially ventilated with a ventilator set to deliver a tidal volume of 30 mL/kg (14 mL/lb) at a rate of 4 breaths/min. RESULTS: Mean +/- SD MAC values during the 3 trials (2 without and 1 with butorphanol) were 2.0 +/- 0.6, 2.1 +/- 0.6, and 1.7 +/- 0.7%, respectively, which were not significantly different from each other. Heart rate and end-tidal partial pressure of CO2 were also not significantly different among the 3 trials. Mean +/- SD heart rate was 48 +/- 10 beats/min; mean end-tidal partial pressure of CO2 was 22 +/- 10 mm Hg.There were no significant differences in blood-gas values for samples obtained at the beginning versus the end of the anesthetic period. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that the MAC of isoflurane in green iguanas is 2.1% and that butorphanol does not have any significant isoflurane-sparing effects.     

Cardiovascular effects of desflurane following acute hemorrhage in dogs

Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end‐tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO₂), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO₂, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO₂ increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO₂ increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage.     

Effects of perzinfotel on the minimum alveolar concentration of isoflurane in dogs

OBJECTIVE: To determine the effect of IV administration of perzinfotel on the minimum alveolar concentration (MAC) of isoflurane in dogs. Animals-6 healthy sexually intact male Beagles. PROCEDURES: Dogs were instrumented with a telemetry device that permitted continuous monitoring of heart rate, arterial blood pressure, and body temperature. Dogs were anesthetized with propofol (4 to 6 mg/kg, IV) and isoflurane for 30 minutes before determination of MAC of isoflurane. Isoflurane MAC values were determined 4 times, separated by a minimum of 7 days, before and after IV administration of perzinfotel (0 [control], 5, 10, and 20 mg/kg). Bispectral index and percentage hemoglobin saturation with oxygen (SpO(2)) were monitored throughout anesthesia. RESULTS: Isoflurane MAC was 1.32 +/- 0.14%. Intravenous administration of perzinfotel at 0, 5, 10, and 20 mg/kg decreased isoflurane MAC by 0%, 24%, 30%, and 47%, respectively. Perzinfotel significantly decreased isoflurane MAC values, compared with baseline and control values. The bispectral index typically increased with higher doses of perzinfotel and lower isoflurane concentrations, but not significantly. Heart rate, body temperature, and SpO(2) did not change, but systolic, mean, and diastolic arterial blood pressures significantly increased with decreases in isoflurane MAC after administration of perzinfotel at 10 and 20 mg/kg, compared with 0 and 5 mg/kg. CONCLUSIONS AND CLINICAL RELEVANCE: IV administration of perzinfotel decreased isoflurane MAC values. Improved hemodynamics were associated with decreases in isoflurane concentration.     

Effects of morphine,lidocaine, ketamine,and morphine-lidocaine-ketamine drug combination on minimum alveolar concentration in dogs anesthetized with isoflurane

OBJECTIVE: To determine the effects of constant rate infusion of morphine, lidocaine, ketamine, and morphine-lidocaine-ketamine (MLK) combination on end-tidal isoflurane concentration (ET-Iso) and minimum alveolar concentration (MAC) in dogs anesthetized with isoflurane and monitor depth of anesthesia by use of the bispectral index (BIS). ANIMALS: 6 adult dogs. PROCEDURE: Each dog was anesthetized with isoflurane on 5 occasions, separated by a minimum of 7 to 10 days. Individual isoflurane MAC values were determined for each dog. Reduction in isoflurane MAC, induced by administration of morphine (3.3 microg/kg/min), lidocaine (50 microg/kg/min), ketamine (10 microg/kg/min), and MLK, was determined. Heart rate, mean arterial blood pressure, oxygen saturation as measured by pulse oximetry (Spo2), core body temperature, and BIS were monitored. RESULTS: Mean +/- SD isoflurane MAC was 1.38 +/- 0.08%. Morphine, lidocaine, ketamine, and MLK significantly lowered isoflurane MAC by 48, 29, 25, and 45%, respectively. The percentage reductions in isoflurane MAC for morphine and MLK were not significantly different but were significantly greater than for lidocaine and ketamine. The Spo2, mean arterial pressure, and core body temperature were not different among groups. Heart rate was significantly decreased at isoflurane MAC during infusion of morphine and MLK. The BIS was inversely related to the ET-Iso and was significantly increased at isoflurane MAC during infusions of morphine and ketamine, compared with isoflurane alone. CONCLUSIONS AND CLINICAL RELEVANCE: Low infusion doses of morphine, lidocaine, ketamine, and MLK decreased isoflurane MAC in dogs and were not associated with adverse hemodynamic effects. The BIS can be used to monitor depth of anesthesia.     

The effects of intrathoracic pressure during continuous two-lung ventilation for thoracoscopy on the cardiorespiratory parameters in sevoflurane anaesthetized dogs

The cardiopulmonary effects of different levels of carbon dioxide insufflation (3, 5 and 2 mm Hg) under two-lung ventilation were studied in six sevoflurane (1.5 minimum alveolar concentration; MAC) anaesthetized dogs during left-sided thoracoscopy. An arterial catheter, Swan-Ganz catheter and multianaesthetic gas analyser were used to monitor the cardiopulmonary parameters during the experiment. Baseline data were obtained before intrathoracic pressure elevation and the measurements were repeated at intervals after left lung collapse induced by insufflation with carbon dioxide gas. The intrapleural pressure levels used were 3, 5 and 2 mm Hg. Arterial blood pressures, cardiac index, stroke index, left and right ventricular stroke work index, arterial haemoglobin saturation, arterial oxygen tension and systemic vascular resistance decreased significantly during hemithorax insufflation, whereas heart rate, right atrial pressure, mean, systolic and diastolic pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance and arterial carbon dioxide tension significantly increased during intrapleural pressure elevation. Although carbon dioxide insufflation into the left hemithorax with an intrapleural pressure of 2-5 mm Hg compromises cardiac functioning in 1.5 MAC sevoflurane anaesthetized dogs, it can be an efficacious adjunct for thoracoscopic procedures. Intrathoracic view was satisfactory with an intrapleural pressure of 2 mm Hg. Therefore, the intrathoracic pressure rise during thoracoscopy with two-lung ventilation should be kept as low as possible. Additional insufflation periods should be avoided, since a more rapid and more severe cardiopulmonary depression can occur.     

Assessment of halothane and sevoflurane anesthesia in spontaneously breathing rats

OBJECTIVE: To characterize halothane and sevoflurane anesthesia in spontaneously breathing rats. ANIMALS: 16 healthy male Sprague-Dawley rats. PROCEDURE: 8 rats were anesthetized with halothane and 8 with sevoflurane. Minimum alveolar concentration (MAC) was determined. Variables were recorded at anesthetic concentrations of 0.8, 1.0, 1.25, and 1.5 times the MAC of halothane and 1.0, 1.25, 1.5, and 1.75 times the MAC of sevoflurane. RESULTS: Mean (+/- SEM) MAC for halothane was 1.02 +/- 0.02% and for sevoflurane was 2.99 +/- 0.19%. As sevoflurane dose increased from 1.0 to 1.75 MAC, mean arterial pressure (MAP) decreased from 103.1 +/- 5.3 to 67.9 +/- 4.6 mm Hg, and PaCO2 increased from 58.8 +/- 3.1 to 92.2 +/- 9.2 mm Hg. As halothane dose increased from 0.8 to 1.5 MAC, MAP decreased from 99 +/- 6.2 to 69.8 +/- 4.5 mm Hg, and PaCO2 increased from 59.1 +/- 2.1 to 75.9 +/- 5.2 mm Hg. Respiratory rate decreased in a dose-dependent fashion from 88.5 +/- 4.5 to 58.5 +/- 2.7 breaths/min during halothane anesthesia and from 42.3 +/- 1.8 to 30.5 +/- 4.5 breaths/min during sevoflurane anesthesia. Both groups of rats had an increase in eyelid and pupillary aperture with an increase in anesthetic dose. CONCLUSIONS AND CLINICAL RELEVANCE: An increase in PaCO2 and a decrease in MAP are clinical indicators of an increasing halothane and sevoflurane dose in unstimulated spontaneously breathing rats. Increases in eyelid aperture and pupil diameter are reliable signs of increasing depth of halothane and sevoflurane anesthesia. Decreasing respiratory rate is a clinical indicator of an increasing dose of halothane.     

Effects of butorphanol and carprofen on the minimal alveolar concentration of isoflurane in dogs

OBJECTIVE: To evaluate the effects of butorphanol and carprofen, alone and in combination, on the minimal alveolar concentration (MAC) of isoflurane in dogs. DESIGN: Randomized complete-block crossover study. ANIMALS: 6 healthy adult dogs. PROCEDURE: Minimal alveolar concentration of isoflurane was determined following administration of carprofen alone, butorphanol alone, carprofen and butorphanol, and neither drug (control). Anesthesia was induced with isoflurane in oxygen, and MAC was determined by use of a tail clamp method. Three hours prior to induction of anesthesia, dogs were fed a small amount of canned food without any drugs (control) or with carprofen (2.2 mg/kg of body weight [1 mg/lb]). Following initial determination of MAC, butorphanol (0.4 mg/kg [0.18 mg/lb], i.v.) was administered, and MAC was determined again. Heart rate, respiratory rate, indirect arterial blood pressure, endtidal partial pressure of CO2, and saturation of hemoglobin with oxygen were recorded at the time MAC was determined. RESULTS: Mean +/- SD MAC of isoflurane following administration of butorphanol alone (1.03 +/- 0.22%) or carprofen and butorphanol (0.90 +/- 0.21%) were significantly less than the control MAC (1.28 +/- 0.14%), but MAC after administration of carprofen alone (1.20 +/- 0.13%) was not significantly different from the control value. The effects of carprofen and butorphanol on the MAC of isoflurane were additive. There were not any significant differences among treatments in regard to cardiorespiratory data. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of butorphanol alone or in combination with carprofen significantly reduces the MAC of isoflurane in dogs; however, the effects of butorphanol and carprofen are additive, not synergistic.     

Effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and clinicopathologic variables in horses

OBJECTIVE: To quantitate the effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and identify changes in selected clinicopathologic variables and serum fluoride values associated with desflurane anesthesia in horses. ANIMALS: 6 healthy adult horses. PROCEDURE: Horses were anesthetized on 2 occasions: first, to determine the minimum alveolar concentration (MAC) of desflurane in O2 and second, to characterize cardiopulmonary and clinicopathologic responses to 1X, 1.5X, and 1.75X desflurane MAC during both controlled and spontaneous ventilation. RESULTS: Mean +/- SEM MAC of desflurane in horses was 8.06 +/- 0.41 %; inhalation of desflurane did not appear to cause airway irritation. During spontaneous ventilation, mean PaCO2 was 69 mm Hg. Arterial blood pressure, stroke volume, and cardiac output decreased as the dose of desflurane increased. Conditions of intermittent positive pressure ventilation and eucapnia resulted in further cardiovascular depression. Horses recovered quickly from anesthesia with little transient or no clinicopathologic evidence of adverse effects. Serum fluoride concentration before and after administration of desflurane was below the limit of detection of 0.05 ppm (2.63microM/L). CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that desflurane, like other inhalation anesthetics, causes profound hypoventilation in horses. The magnitude of cardiovascular depression is related to dose and mode of ventilation; cardiovascular depression is less severe at doses of 1X to 1.5X MAC, compared with known effects of other inhalation anesthetics under similar conditions. Desflurane is not metabolized to an important degree and does not appear to prominently influence renal function or hepatic cellular integrity or function.     

Effect of morphine and flunixin meglumine on isoflurane minimum alveolar concentration in goats

OBJECTIVE: To determine the effect of morphine and flunixin meglumine on isoflurane (ISO) minimum alveolar concentration (MAC) in goats. STUDY DESIGN: Prospective, randomized experimental study. ANIMALS: Five adult, wether goats from 1 to 3 years in age, and weighing 24-65 kg. METHODS: Anesthesia was induced using ISO, which was delivered via a mask. Goats were intubated and ventilated to maintain an end-tidal carbon dioxide concentration between 25 and 30 mm Hg (3.3-4 kPa). End-tidal ISO concentration was measured using an infrared analyzer. The baseline ISO MAC that prevented purposeful movement in response to clamping a claw was determined. Following baseline MAC determination, each goat received one of the following four treatments intravenously (IV): morphine (2 mg kg(-1)), flunixin (1.5 mg kg(-1)), flunixin (1.5 mg kg(-1)) plus morphine (2 mg kg(-1)) or saline, and the MAC was re-determined. Goats were studied at weekly intervals, and each goat received each treatment in a randomized fashion. RESULTS: The baseline ISO MAC for the control treatment was 1.43%. Morphine reduced the MAC by 29.7%. Flunixin did not significantly decrease the MAC nor did it potentiate the effect of morphine on MAC. The quality of recovery was good in all cases. CONCLUSIONS: Morphine (2 mg kg(-1), IV) significantly reduced the ISO MAC in goats and did not adversely affect the quality of recovery. CLINICAL RELEVANCE: The use of morphine, at the dose studied, in association with ISO anesthesia, will allow a clinically significant reduction in the concentration of ISO required to maintain general anesthesia in goats.     

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.     

Effects of adenosine infusion on the minimum alveolar concentration of isoflurane in dogs

OBJECTIVE: To determine the effects of adenosine infusion on the minimum alveolar concentration (MAC) of isoflurane in dogs. STUDY DESIGN: Prospective, randomized crossover study. ANIMALS: Seven adult male and female Beagles weighing 10.9 (7.5, 13.6) kg [median (minimum, maximum)]. METHODS: Each dog was anesthetized with isoflurane in oxygen and randomly assigned to receive either an intravenous (IV) adenosine (0.3 mg kg(-1) minute(-1)) or saline (6 mL kg(-1) hour(-1) IV) infusion. After an interval of 7 days or more, each dog was re-anesthetized and treated with the alternative infusion. Using a tail-clamp technique, MAC was determined before (pre-infusion), during (infusion), and 2 hours after the infusions (post-infusion). RESULTS: The pre-infusion MAC of isoflurane was 1.25 (1.15, 1.35) [median (minimum, maximum)] vol.% for the saline treatment group and 1.25 (1.05, 1.45) vol.% for the adenosine treatment group, and did not differ significantly between the two treatments. The infusion MAC values were not significantly different (p = 0.16) and were 1.25 (0.95, 1.35) vol.% and 1.05 (1.00, 1.25) vol.%, respectively. The post-infusion MAC values differed significantly (p = 0.016); MAC was 1.15 (1.15, 1.35) vol.% and 1.05 (1.05, 1.25) vol.% for the saline and adenosine treatment groups, respectively. During infusion, mean arterial blood pressure decreased significantly (p = 0.008) during adenosine treatment compared with the saline 66 mmHg (52, 72) and 91 mmHg (68, 110), respectively. End-tidal CO2 (Pe'CO2), urine production, hematocrit, and plasma total solids did not differ significantly between the two treatments at any time (all p > 0.05). CONCLUSION: Although the MAC of isoflurane in dogs was not decreased significantly during infusion with adenosine (0.3 mg kg(-1) minute(-1)), it was significantly decreased post-infusion, but only by 0.1 vol.%, an amount not considered clinically important. Adenosine infusion decreased mean arterial pressure by 27% and did not adversely affect renal function.     

Sparing effect of tramadol,lidocaine, dexmedetomidine and their combination on the minimum alveolar concentration of sevoflurane in dogs

BackgroundProblems associated with using inhalational anaesthesia are numerous in veterinary anaesthesia practice. Decreasing the amount of used inhalational anaesthetic agents and minimising of cardiorespiratory disorders are the standard goals of anaesthetists.ObjectiveThis experimental study was carried out to investigate the sparing effect of intravenous tramadol, lidocaine, dexmedetomidine and their combinations on the minimum alveolar concentration (MAC) of sevoflurane in healthy Beagle dogs.MethodsThis study was conducted on six beagle dogs. Sevoflurane MAC was determined by the tail clamp method on five separate occasions. The dogs received no treatment (control; CONT), tramadol (TRM: 1.5 mg kg^-1 intravenously followed by 1.3 mg kg^-1 h^-1), lidocaine (LID: 2 mg kg^-1 intravenously followed by 3 mg kg^-1 h^-1), dexmedetomidine (DEX: 2 μg kg^-1 intravenously followed by 2 μg kg^-1 h^-1), and their combination (COMB), respectively. Cardiorespiratory variables were recorded every five minutes and immediately before the application of a noxious stimulus.ResultsThe COMB treatment had the greatest sevoflurane MAC-sparing effect (67.4 ± 13.9%) compared with the other treatments (5.1 ± 25.3, 12.7 ± 14.3, and 40.3 ± 15.1% for TRM, LID, and DEX treatment, respectively). The cardiopulmonary variables remained within the clinically acceptable range following COMB treatment, although the mean arterial pressure was higher and accompanied by bradycardia.ConclusionsTramadol-lidocaine-dexmedetomidine co-infusion produced a remarkable sevoflurane MAC-sparing effect in clinically healthy beagle dogs and could result in the alleviation of cardiorespiratory depression caused by sevoflurane. Cardiorespiratory variables should be monitored carefully to avoid undesirable side effects induced by dexmedetomidine.     

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.     

Determination of the minimum anesthetic concentration and cardiovascular dose response for sevoflurane in chickens during controlled ventilation

OBJECTIVE: To determine the minimum anesthetic concentration for sevoflurane and effects of various multiples of minimum anesthetic concentration on arterial pressure and heart rate during controlled ventilation in chickens. STUDY DESIGN: Prospective experimental study. ANIMALS: Seven healthy chickens, 6 to 8 months old, weighing 1.6 to 3.4 kg. METHODS: A rebreathing, semiclosed anesthetic circuit was used. Anesthesia was induced by mask with sevoflurane in oxygen. Each chicken was endotracheally intubated, then controlled ventilation was started and the end-tidal CO2 partial pressure was maintained at 30 to 40 mm Hg. Body temperature was maintained at 39.5 degrees to 41.0 degrees C. The inspired and end-tidal sevoflurane concentration were monitored with a multigas monitor. Minimum anesthetic concentration was determined as the minimal end-tidal sevoflurane concentration which prevented gross purposeful movement in response to clamping a toe for 1 minute. After the determination, the cardiovascular effects of sevoflurane at 1.0, 1.5, and 2.0 times the minimum anesthetic concentration were determined. RESULTS: The minimum anesthetic concentration for sevoflurane was 2.21% + 0.32% (mean +/- SD). Mean arterial pressure and heart rate at minimum anesthetic concentration were 84 +/- 13 mm Hg and 150 +/- 58 beats/min, respectively. There was a dose-dependent decrease in arterial pressure. The heart rate did not change significantly over the range 1 to 2 x minimum anesthetic concentration. No cardiac arrhythmias developed throughout the experiments. CONCLUSIONS AND CLINICAL RELEVANCE: The minimum anesthetic concentration for sevoflurane in chickens was within the range of minimum alveolar concentration reported in mammals. When the concentration of sevoflurane is increased during controlled ventilation in chickens, decrease in arterial pressure should be expected.     

Effects of epidural administration of dexmedetomidine on the minimum alveolar concentration of isoflurane in dogs

Objective-To evaluate the effects of epidural administration of 3 doses of dexmedetomidine on isoflurane minimum alveolar concentration (MAC) and characterize changes in bispectral index (BIS) induced by nociceptive stimulation used for MAC determination in dogs. Animals-6 adult dogs. Procedures-Isoflurane-anesthetized dogs received physiologic saline (0.9% NaCl) solution (control treatment) or dexmedetomidine (1.5 [DEX1.5], 3.0 [DEX3], or 6.0 [DEX6] mug/kg) epidurally in a crossover study. Isoflurane MAC (determined by use of electrical nociceptive stimulation of the hind limb) was targeted to be accomplished at 2 and 4.5 hours. Changes in BIS attributable to nociceptive stimulation and cardiopulmonary data were recorded at each MAC determination. Results-With the control treatment, mean +/- SD MAC values did not change over time (1.57 +/- 0.23% and 1.55 +/- 0.25% at 2 and 4.5 hours, respectively). Compared with the control treatment, MAC was significantly lower at 2 hours (13% reduction) but not at 4.5 hours (7% reduction) in DEX1.5-treated dogs and significantly lower at 2 hours (29% reduction) and 4.5 hours (13% reduction) in DEX3-treated dogs. The DEX6 treatment yielded the greatest MAC reduction (31% and 22% at 2 and 4.5 hours, respectively). During all treatments, noxious stimulation increased BIS; but changes in BIS were correlated with increases in electromyographic activity. Conclusions and Clinical Relevance-In dogs, epidural administration of dexmedetomidine resulted in dose-dependent decreases in isoflurane MAC and that effect decreased over time. Changes in BIS during MAC determinations may not represent increased awareness because of the possible interference of electromyographic activity.     

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

OBJECTIVE: To determine the influence of a low-dose constant rate infusion (LCRI; 50 microg kg(-1) minute(-1)) and high-dose CRI (HCRI; 200 microg kg(-1) minute(-1)) lidocaine infusion on the minimum alveolar concentration (MAC) of isoflurane (I) in dogs. STUDY DESIGN: Prospective experimental study. ANIMALS: Ten mongrel dogs (four females, six males), weighing 20-26.3 kg. METHODS: Dogs were anesthetized with I in oxygen and their lungs mechanically ventilated. Baseline MAC was determined using mechanical or electrical stimuli. Lidocaine (2 mg kg(-1) IV) was administered over 3 minutes, followed by the LCRI and MAC determination commenced 30 minutes later. Once MAC was determined following LCRI, the lidocaine infusion was stopped for 30 minutes. A second bolus of lidocaine (2 mg kg(-1), IV) was administered, followed by the HCRI and MAC re-determined. Concentrations of lidocaine and its metabolites were measured at end-tidal I concentrations immediately above and below MAC. Heart rates and blood pressures were measured. RESULTS: Minimum alveolar concentration of I was 1.34 +/- 0.11 (%; mean +/- SD) for both types of stimulus. The LCRI significantly reduced MAC to 1.09 +/- 0.13 (18.7% reduction) and HCRI to 0.76 +/- 0.10 (43.3% reduction). Plasma concentrations (ng mL(-1), median; value below and above MAC, respectively) for LCRI were: lidocaine, 1465 and 1537; glycinexylidide (GX), 111 and 181; monoethylglycinexylidide (MEGX), 180 and 471 and for HCRI were: lidocaine, 4350 and 4691; GX, 784 and 862; MEGX, 714 and 710. Blood pressure was significantly increased at 30 minutes after high dose infusion. CONCLUSION AND CLINICAL RELEVANCE: Lidocaine infusions reduced the MAC of I in a dose-dependent manner and did not induce clinically significant changes on heart rate or blood pressure.