The effect of hypovolemia due to hemorrhage on the minimum alveolar concentration of isoflurane in the dog

OBJECTIVE: To determine the effect of hypovolemia on the minimum alveolar concentration (MAC) of isoflurane in the dog. STUDY DESIGN: Randomized, cross-over trial. ANIMAL POPULATION: Six healthy intact mixed breed female dogs weighing 18.2-29.0 kg. METHODS: Dogs were randomly assigned to determine the MAC of isoflurane in a normovolemic or hypovolemic state with a minimum of 18 days between trials. On both occasions, anesthesia was initially induced and maintained for 40 minutes with isoflurane delivered in oxygen while vascular catheters were placed in the cephalic vein and dorsal metatarsal artery. In dogs assigned to the hypovolemic group, 30 mL kg(-1) of blood was removed at 1 mL kg(-1) minute(-1) from the arterial catheter. All dogs were allowed to recover from anesthesia. Thirty minutes after the discontinuation of isoflurane, anesthesia was re-induced with isoflurane in oxygen delivered by face mask. The tracheas were intubated, and connected to an anesthetic machine with a Bain anesthetic circuit. Mechanical ventilation was instituted at a rate of 10 breaths minute(-1) with the tidal volume set to deliver 10-15 mL kg(-1). Airway gases were monitored continuously and tidal volume was adjusted to maintain an end-tidal carbon dioxide level of 35-40 mmHg (4.67-5.33 kPa). Body temperature was maintained at 37-38 degrees C (98.6-100.4 degrees F). The MAC determination was performed using an electrical stimulus applied to the toe web and MAC was defined as the mean value of end-tidal isoflurane between the concentrations at which a purposeful movement did and did not occur in response to the electrical stimulus. The MAC values were compared between groups using a Student's t-test. RESULTS: The MAC of isoflurane was significantly less in hypovolemic dogs (0.97 +/- 0.03%) compared with normovolemic dogs (1.15 +/- 0.02%) (p < 0.0079). CONCLUSIONS AND CLINICAL RELEVANCE: The MAC of isoflurane is reduced in dogs with hypovolemia resulting from hemorrhage. Veterinarians should be prepared to deliver a lower percentage of isoflurane to maintain anesthesia in hypovolemic dogs during diagnostic and therapeutic procedures.     

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.     

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.     

Alterations in epinephrine-induced arrhythmogenesis after xylazine and subsequent yohimbine administration in isoflurane-anesthetized dogs

Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.     

Comparison of romifidine and medetomidine pre-medication in propofol-isoflurane anaesthetised dogs

The objective of this paper was to evaluate romifidine as a pre-medicant in dogs prior to propofol-isoflurane anaesthesia, and to compare it with medetomidine. For this, eight healthy dogs were anaesthetised. Each dog received three pre-anaesthetic protocols: R40 (romifidine, 40 microg/kg, IV), R80 (romifidine, 80 microg/kg, IV) or MED (medetomidine, 10 microg/kg, IV). Induction of anaesthesia was delivered with propofol and maintained with isoflurane. The following variables were studied before sedative administration and 10 min after sedative administration: heart rate (HR), mean arterial pressure (MAP), systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) and respiratory rate (RR). During maintenance, the following variables were recorded at 5-min intervals: HR, MAP, SAD, DAP, arterial oxygen saturation (SpO(2)), end-tidal CO(2)(EtCO(2)), end-tidal concentration of isoflurane (EtISO) required for maintenance of anaesthesia and tidal volume (TV). Time to extubation, time to sternal recumbency and time to standing were also registered. HR and RR experimented a significantly decreased during sedation in all protocols respect to baseline values. Mean HR, MAP, SAP, DAP, SpO(2), EtCO(2), and TV during anaesthesia were similar for the three protocols. End tidal of isoflurane concentration was statistically similar for all protocols. Recovery time for R40 was significantly shorter than in R80 and MED. The studied combination of romifidine, propofol and isoflurane appears to be an effective drug combination for inducing and maintaining general anaesthesia in healthy dogs.     

The effects of propofol, isoflurane and sevoflurane on vecuronium infusion rates for surgical muscle relaxation in dogs

OBJECTIVE: To compare the constant rate infusion (CRI) of vecuronium required to maintain a level of neuromuscular blockade adequate for major surgeries, e.g. thoracotomy or laparotomy, in dogs anaesthetized with a CRI of fentanyl and either propofol, isoflurane or sevoflurane. STUDY DESIGN: Prospective, randomized, cross-over study. ANIMALS: Thirteen male beagles (age, 9-22 months; body mass 6.3-11.3 kg). MATERIALS AND METHODS: Dogs were anaesthetized with propofol (24 mg kg(-1) hour(-1) IV CRI; group P), isoflurane (1.3% end-tidal concentration; group I) or sevoflurane (2.3% end-tidal concentration; group S) with fentanyl (5 microg kg(-1) hour(-1) IV, CRI). Sixty to seventy minutes after induction of anaesthesia, vecuronium was administered at a rate of 0.4, 0.3 and 0.2 mg kg(-1) hour(-1) in groups P, I and S respectively. To determine the degree of neuromuscular block, a peripheral nerve was stimulated electrically using the train-of-four (TO4) stimulus pattern. Evoked muscle contractions were evaluated using a neuromuscular monitoring device. Once the TO4 ratio reached 0, the continuous infusion rate was decreased and adjusted to maintain a TO4 count of 1. Continuous infusion was continued for 2 hours. The infusion rate of vecuronium was recorded 20, 40, 60, 80, 100 and 120 minutes after the start of infusion. RESULTS: The mean continuous infusion rates of vecuronium during stable infusion were 0.22 +/- 0.04 (mean +/- SD), 0.10 +/- 0.02 and 0.09 +/- 0.02 mg kg(-1) hour(-1) in groups P, I and S respectively. There were statistically significant differences between the rates in groups P and I and between the rates in groups P and S. Conclusions and clinical relevance In healthy dogs, the recommended maintenance infusion rate of vecuronium is 0.2 mg kg(-1) hour(-1) under CRI propofol-fentanyl anaesthesia and 0.1 mg kg(-1) hour(-1) during CRI fentanyl-isoflurane or sevoflurane anaesthesia.     

Changes in the minimum alveolar concentration of isoflurane and some cardiopulmonary measurements during three continuous infusion rates of dexmedetomidine in dogs

OBJECTIVE: To measure the change in the minimum alveolar concentration of isoflurane associated with three constant rate infusions of dexmedetomidine. STUDY DESIGN: Prospective, randomized, and blinded experimental trial. Animals Six healthy 6-year-old Beagles weighing between 13.0 and 17.7 kg. METHODS: The dogs received each of four treatments; saline or dexmedetomidine at 0.1, 0.5 or 3 microg kg(-1) loading dose given intravenously (IV) over 6 minutes followed by infusions at 0.1, 0.5 or 3 microg kg(-1) hour(-1), respectively. There were 2 weeks between treatments. The dogs were mask-induced with and maintained on isoflurane in oxygen. Acetated Ringer's (5 mL kg(-1) hour(-1)) and saline or dexmedetomidine (each at 0.5 mL kg(-1) hour(-1)) were given IV. Pulse rate, blood pressure, samples for the measurement of blood gases, pH, lactate, packed cell volume (PCV), total protein (TP) and dexmedetomidine concentrations were obtained from an arterial catheter. Sixty minutes after induction minimum alveolar concentration (MAC) was determined by intermittently applying supramaximal electrical stimuli to the thoracic and pelvic limbs. Cardiopulmonary measurements and arterial blood samples were collected before each set of stimuli. Statistical analyses were conducted with analysis of variance or mixed models according to the experimental design. RESULTS: There was a significant decrease in the MAC of isoflurane associated with 0.5 and 3 microg kg(-1) hour(-1) but not with 0.1 mg kg(-1)hour(-1). Serum concentrations of dexmedetomidine were not measurable at the 0.1 mg kg(-1) hour(-1) and averaged 0.198 +/- 0.081 and 1.903 +/-0.621 ng mL(-1) for the 0.5 and 3 microg kg(-1) hour(-1) infusion rates, respectively. Heart rate decreased with increasing doses of dexmedetomidine while blood pressure increased. Packed cell volume increased at 3 microg kg(-1) hour(-1) but not with other doses. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine infusions decrease the intra-operative requirement for isoflurane and may be useful in managing dogs undergoing surgery, where the provision of analgesia and limitation of the stress response is desirable.     

Comparison of sevoflurane and isoflurane in dogs anaesthetised for clinical surgical or diagnostic procedures

OBJECTIVES: To assess attributes of sevoflurane for routine clinical anaesthesia in dogs by comparison with the established volatile anaesthetic isoflurane. METHODS: One hundred and eight dogs requiring anaesthesia for elective surgery or diagnostic procedures were studied. The majority was premedicated with 0.03 mg/kg of acepromazine and 0.01 mg/kg of buprenorphine or 0.3 mg/kg of methadone before induction of anaesthesia with 2 to 4 mg/kg of propofol and 0.5 mg/kg of diazepam. They were randomly assigned to receive either sevoflurane (group S, n=50) or isoflurane (group I, n=58) in oxygen and nitrous oxide for maintenance of anaesthesia. Heart rate, respiratory rate, indirect arterial blood pressure, haemoglobin saturation, vaporiser settings, end-tidal carbon dioxide and anaesthetic concentration and oesophageal temperature were measured. Recovery was timed. Data were analysed using analysis of variance and non-parametric tests. RESULTS: Heart rate (85 to 140/minute), respiratory rate (six to 27/minute) and systolic arterial blood pressure (80 to 150 mmHg) were similar in the two groups. End-tidal carbon dioxide between 30 and 60 minutes (group S 6.4 to 6.6 and group I 5.8 to 5.9 per cent) and vaporiser settings throughout (group S 2.1 to 2.9 and group I 1.5 to 1.5 per cent) were higher in group S. There was no difference in time to head lift (18+/-16 minutes), sternal recumbency (28+/-22 minutes) or standing (48+/-32 minutes). No adverse events occurred. CLINICAL SIGNIFICANCE: Sevoflurane appeared to be a suitable volatile anaesthetic for maintenance of routine clinical anaesthesia in dogs.     

Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs

OBJECTIVE: To evaluate the effects of acepromazine maleate on the cardiovascular changes induced by dopamine in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, randomized cross-over experimental design. ANIMALS: Six healthy adult spayed female dogs weighing 16.4 +/- 3.5 kg (mean +/- SD). METHODS: Each dog received two treatments, at least 1 week apart. Acepromazine (0.03 mg kg(-1), IV) was administered 15 minutes before anesthesia was induced with propofol (7 mg kg(-1), IV) and maintained with isoflurane (1.8% end-tidal). Acepromazine was not administered in the control treatment. Baseline cardiopulmonary parameters were measured 90 minutes after induction. Thereafter, dopamine was administered intravenously at 5, 10, and 15 microg kg(-1) minute(-1), with each infusion rate lasting 30 minutes. Cardiopulmonary data were obtained at the end of each infusion rate. RESULTS: Dopamine induced dose-related increases in cardiac index (CI), stroke index, arterial blood pressure, mean pulmonary arterial pressure, oxygen delivery index (DO(2)I) and oxygen consumption index. In the control treatment, systemic vascular resistance index (SVRI) decreased during administration of 5 and 10 microg kg(-1) minute(-1) of dopamine and returned to baseline with the highest dose (15 microg kg (-1) minute(-1)). After acepromazine treatment, SVRI decreased from baseline during dopamine administration, regardless of the infusion rate, and this resulted in a smaller increase in blood pressure at 15 microg kg (-1) minute(-1). During dopamine infusion hemoglobin concentrations were lower following acepromazine and this contributed to significantly lower arterial O(2) content. CONCLUSIONS: Acepromazine prevented the return in SVRI to baseline and reduced the magnitude of the increase in arterial pressure induced by higher doses of dopamine. However, reduced SRVI associated with lower doses of dopamine and the ability of dopamine to increase CI and DO(2)I were not modified by acepromazine premedication. CLINICAL RELEVANCE: Previous acepromazine administration reduces the efficacy of dopamine as a vasopressor agent in isoflurane anesthetized dogs. Other beneficial effects of dopamine such as increased CO are not modified by acepromazine.     

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.     

Effects of ketamine and magnesium on the minimum alveolar concentration of isoflurane in goats

OBJECTIVE: To evaluate the effects of ketamine, magnesium sulfate, and their combination on the minimum alveolar concentration (MAC) of isoflurane (ISO-MAC) in goats. ANIMALS: 8 adult goats. PROCEDURES: Anesthesia was induced with isoflurane delivered via face mask. Goats were intubated and ventilated to maintain normocapnia. After an appropriate equilibration period, baseline MAC (MAC(B)) was determined and the following 4 treatments were administered IV: saline (0.9% NaCl) solution (loading dose [LD], 30 mL/20 min; constant rate infusion [CRI], 60 mL/h), magnesium sulfate (LD, 50 mg/kg; CRI, 10 mg/kg/h), ketamine (LD, 1 mg/kg; CRI, 25 microg/kg/min), and magnesium sulfate (LD, 50 mg/kg; CRI, 10 mg/kg/h) combined with ketamine (LD, 1 mg/kg; CRI, 25 microg/kg/min); then MAC was redetermined. RESULTS: Ketamine significantly decreased ISOMAC by 28.7 +/- 3.7%, and ketamine combined with magnesium sulfate significantly decreased ISOMAC by 21.1 +/- 4.1%. Saline solution or magnesium sulfate alone did not significantly change ISOMAC. CONCLUSIONS AND CLINICAL RELEVANCE: Ketamine and ketamine combined with magnesium sulfate, at doses used in the study, decreased the end-tidal isoflurane concentration needed to maintain anesthesia, verifying the clinical impression that ketamine decreases the end-tidal isoflurane concentration needed to maintain surgical anesthesia. Magnesium, at doses used in the study, did not decrease ISOMAC or augment ketamine's effects on ISOMAC.     

Influence of three anesthetic protocols on glomerular filtration rate in dogs

OBJECTIVE: To investigate renal function in clinically normal dogs when awake and during anesthesia with medetomidine; xylazine, ketamine, and halothane (XKH) combination; or propofol. ANIMALS: 10 adult female Beagles. PROCEDURES: At intervals of 15 days, dogs were administered medetomidine (0.05 mg/kg, IV); XKH combination (xylazine [1 mg/kg, IV], ketamine [5 mg/kg, IV], and halothane [1% end-tidal concentration]); or propofol (6 mg/kg, IV) to induce anesthesia or no treatment. Glomerular filtration rate was assessed on the basis of renal uptake (RU; determined via renal scintigraphy) and plasma clearance (CL) of technetium 99m-labeled diethylenetriamine pentaacetic acid ((99m)Tc-DTPA). RESULTS: In awake dogs, mean +/- SEM RU was 9.7 +/- 0.4% and CL was 3.86 +/- 0.23 mL/min/ kg. Renal uptake and CL of (99m)Tc-DTPA were not significantly modified by administration of XKH (RU, 11.4 +/- 0.9%; CL, 4.6 +/- 0.32 mL/min/kg) or propofol (RU, 9.7 +/- 0.3%; CL, 3.78 +/- 0.37 mL/min/kg). Half-life elimination time of plasma (99m)Tc-DTPA decreased significantly in XKH-anesthetized dogs, compared with the value in awake dogs (14.4 minutes and 28.9 minutes, respectively). However, glomerular filtration rate was significantly decreased by administration of medetomidine (RU, 3.9 +/- 0.1%), and the time to maximum kidney activity was significantly increased (867 +/- 56 seconds vs 181 +/- 11 seconds without anesthesia). CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that anesthesia with propofol or an XKH combination did not alter renal function in healthy Beagles, but anesthesia with medetomidine decreased early RU of (99m)Tc-DTPA.     

The effect of remifentanil infusion on sevoflurane minimum alveolar concentration–no movement (MACNM) and bispectral index in dogs

ObjectiveTo determine the effect of remifentanil infusion on the minimum alveolar concentration of sevoflurane preventing movement (SEVOMAC_NM) and bispectral index (BIS) in dogs.Study designProspective, unmasked study.AnimalsA total of 10 adult Beagle dogs weighing 9.0 ± 1.1 kg.MethodsDogs were anesthetized with sevoflurane and baseline SEVOMAC_NM was determined. Remifentanil was infused at 5, 10 and 20 μg kg^–1 hour^–1, in sequence, with 20 minutes washout between infusions. Variables monitored throughout anesthesia included heart rate (HR), oscillometric blood pressure, end-tidal partial pressure of carbon dioxide, end-tidal sevoflurane concentration (Fe′Sevo) and BIS. SEVOMAC_NM after remifentanil infusion (SEVOMAC_NM-REMI) determination started 20 minutes after the start of each infusion. Venous blood samples were collected for plasma remifentanil concentration determination at baseline, SEVOMAC_NM-REMI determination time points, and 20 minutes after each infusion was stopped. A mixed model analysis was used to determine the effect of remifentanil infusion on response variables. The relationships between BIS and Fe′Sevo, plasma remifentanil concentrations and the percentage decrease in baseline SEVOMAC_NM were evaluated (p < 0.05).ResultsThe overall SEVOMAC_NM at baseline was 2.47 ± 0.11%. Addition of remifentanil at all infusion rates significantly decreased SEVOMAC_NM, but the medium and high doses resulted in significantly greater decreases in SEVOMAC_NM than the lower dose. There was no difference in SEVOMAC_NM percentage change between infusions 10 and 20 μg kg^–1 hour^–1. Plasma remifentanil concentrations were significantly different in all infusion rates. Baseline BIS value was 70 ± 1 and was lower than the BIS values recorded during all remifentanil infusions. BIS values were not significantly different among infusion rates. HR was lower and mean arterial pressure was higher during remifentanil infusions than at baseline.Conclusions and clinical relevanceAll remifentanil infusions decreased SEVOMAC_NM in dogs. Remifentanil infusion at any rate studied did not reduce BIS values.     

Evaluation of induction characteristics and hypnotic potency of isoflurane and sevoflurane in healthy dogs

OBJECTIVE: To determine induction characteristics and the minimum alveolar concentration (MAC) at which consciousness returned (MACawake) in dogs anesthetized with isoflurane or sevoflurane. ANIMALS: 20 sexually intact male Beagles. PROCEDURES: In experiment 1, 20 dogs were randomly assigned to have anesthesia induced and maintained with isoflurane or sevoflurane. The MAC at which each dog awoke in response to auditory stimulation (MACawake-noise) was determined by decreasing the end-tidal concentration by 0.1 volume (vol %) every 15 minutes and delivering a standard audible stimulus at each concentration until the dog awoke. In experiment 2, 12 dogs received the same anesthetic agent they were administered in experiment 1. After duplicate MAC determination, the end-tidal concentration was continually decreased by 10% every 15 minutes until the dog awoke from anesthesia (MACawake). RESULTS: Mean induction time was significantly greater for isoflurane-anesthetized dogs (212 seconds), compared with the sevoflurane-anesthetized dogs (154 seconds). Mean+/-SD MACawake-noise was 1.1+/-0.1 vol % for isoflurane and 2.0+/-0.2 vol % for sevoflurane. Mean MAC was 1.3+/-0.2 vol % for isoflurane and 2.1+/-0.6 vol % for sevoflurane, and mean MACawake was 1.0+/-0.1 vol % for isoflurane and 1.3+/-0.3 vol % for sevoflurane. CONCLUSIONS AND CLINICAL RELEVANCE: Sevoflurane resulted in a more rapid induction than did isoflurane. The MACawake for dogs was higher than values reported for both agents in humans. Care should be taken to ensure that dogs are at an appropriate anesthetic depth to prevent consciousness, particularly when single-agent inhalant anesthesia is used.     

Evaluation of an anaesthetic technique used in dogs undergoing craniectomy for tumour resection

ObjeCTIVE: To evaluate a total intravenous anaesthetic technique in dogs undergoing craniectomy. STUDY DESIGN: Prospective clinical study. ANIMALS: Ten dogs admitted for elective surgical resection of rostro-tentorial tumours. METHODS: All dogs were premedicated with methadone, 0.2 mg kg(-1) intramuscularly 30 minutes prior to induction of anaesthesia. Anaesthesia was induced with propofol administered intravenously (IV) to effect, following administration of lidocaine 1 mg kg(-1) IV and maintained with a continuous infusion of propofol at < or =0.4 mg kg(-1) minute(-1) during instrumentation and preparation and during movement of the animals to recovery. During surgery, anaesthesia was maintained using a continuous infusion of propofol at 相似文献   

Investigation of the interaction between buprenorphine and sufentanil during anaesthesia for ovariectomy in dogs

OBJECTIVE: To investigate the effect of buprenorphine pre-treatment on sufentanil requirements in female dogs undergoing ovariectomy. STUDY DESIGN: Randomized, 'blinded', prospective clinical study. ANIMALS: Thirty healthy female dogs referred for ovariectomy. MATERIALS AND METHODS: Dogs were randomly assigned to one of two pre-anaesthetic treatment groups. Those in the buprenorphine group (B) received buprenorphine 20 microg kg(-1) and acepromazine 0.03 mg kg(-1) IM. Control group (C) animals received an equal volume of NaCl 0.9% and acepromazine 0.03 mg kg(-1) IM. The anaesthetic technique was identical in both groups. Pre-anaesthetic medication consisted of intravenous (IV) sufentanil (1.0 microg kg(-1)) and midazolam (0.05 mg kg(-1)) and intramuscular atropine (0.03 mg kg(-1)). Anaesthesia was induced with propofol and maintained with a constant rate infusion of sufentanil (1.0 microg kg(-1) hour(-1)) and with oxygen-isoflurane. Ventilation was controlled mechanically. Ovariectomy was performed using a standard technique. Baseline heart rate (HR) and direct mean arterial blood pressure (MAP) were recorded before the first incision. Increases in HR and MAP of > or =20% over baseline and, or spontaneous ventilation were controlled using IV sufentanil (1.0 microg kg(-1)) repeated after 5 minutes if haemodynamic variables remained elevated or attempts at spontaneous ventilation persisted. Analysis of variance was used to determine group differences in mean and median HR and MAP and to compare the maximum HR and MAP attained during surgery. Poisson regression was used to compare the number of sufentanil injections required in both groups. RESULTS: Group B required 2.46 times more sufentanil injections (p = 0.00487) than dogs in group C to maintain haemodynamic stability and prevent spontaneous ventilation during surgery. Group B dogs also had a significantly higher (p = 0.034) marginal mean of the log maximum MAP (4.756 +/- 0.036) compared with group C (4.642 +/- 0.036). CONCLUSIONS: Pre-treatment with buprenorphine appears to negatively influence the antinociceptive efficacy of intra-operative sufentanil. CLINICAL RELEVANCE: Withholding buprenorphine therapy 6-8 hours before anaesthesia incorporating pure mu receptor agonists is probably advisable. Alternative methods of analgesia should be provided in this period.     

Comparison of intra-operative analgesia provided by intravenous regional anesthesia or brachial plexus block for pancarpal arthrodesis in dogs

The aim of this study was to compare intravenous regional anesthesia (IVRA) and brachial plexus block (BPB) for intra-operative analgesia in dogs undergoing pancarpal arthrodesis (PA). Twenty dogs scheduled for PA were intramuscularly sedated with acepromazine (0.03mg/kg), general anesthesia was intravenously (IV) induced with thiopental (10mg/kg) and, after intubation, maintained with isoflurane in oxygen. In 10 dogs (GIVRA) IVRA was performed on the injured limb administering 0.6ml/kg of 0.5% lidocaine. In 10 dogs (GBPB) the BPB was performed at the axillary level with the help of a nerve stimulator and 0.3ml/kg of a 1:1 solution of 2% lidocaine and 1% ropivacaine was injected. During surgery fentanyl (0.002mg/kg IV) was administered if there was a 15% increase of HR and/or MAP compared to the values before surgical stimulation. All the standard cardiovascular and respiratory parameters were continuously monitored during surgery. The duration of surgery and the time of extubation were recorded. Data were compared with a 1-way ANOVA test (P<0.05). No patients required fentanyl administration during surgery. All the recorded parameters were similar in the two groups. The two techniques were similar in providing intra-operative analgesia in dogs undergoing orthopaedic surgery.     

Clinical investigation of remifentanil and propofol for the total intravenous anaesthesia of dogs

Fifteen adult dogs underwent elective ovariectomy. They were premedicated with 0.5 mg/kg methadone and 0.05 mg/kg(-1) atropine administered intramuscularly, and anaesthesia was induced with propofol and maintained with intravenous infusions of remifentanil at 0.6 microg/kg/minute and propofol; the mean (sd) rate of infusion of propofol throughout the period of anaesthesia was 0.33 (0.03) mg/kg/minute. The dogs were ventilated continuously with oxygen while they were anaesthetised. Their haemodynamic parameters were clinically acceptable during the period of anaesthesia. Two dogs received additional atropine to correct bradycardias of less than 60 bpm and several dogs received additional boluses of remifentanil or propofol to maintain an adequate depth of anaesthesia, as determined by a clinical assessment. The mean (range) time to the return of spontaneous respiration after stopping the remifentanil infusion was 11.1 (6.0 to 17.0) minutes, and the mean (range) time to the dogs standing was 38.0 (20.0 to 80.0) minutes. The quality of recovery was good in 12 of the dogs, two showed mild excitation in the immediate postoperative period and the other dog required additional analgesia with methadone.     

Normal values and incidence of cardiorespiratory complications in dogs during general anaesthesia. A review of 1281 cases

This paper describes the cardiorespiratory variables and the incidence of anaesthetic complications in dogs. For this, a retrospective study of 1281 anaesthesias was performed. Heart rate (HR), non-invasive mean arterial (MAP), systolic (SP) and diastolic pressures (DP), invasive mean arterial (IMAP), systolic (ISP) and diastolic pressures (IDP), central venous pressure (CVP), respiratory rate (RR), tidal volume (V(T)), minute volume (V(M)), end-tidal CO(2) (EtCO(2)), arterial oxygen saturation (SpO(2)), temperature (T) and death are reported. Data were described both globally and separately for each ASA (American Society of Anaesthesiologists classification) status. An ANOVA and a Tukey's test were used for comparing the different ASA status' values (alpha=0.05). During anaesthetic maintenance, the mean +/- SD of the studied variables were: HR: 91+/-27 bpm. MAP: 86+/-24 mmHg. IMAP: 80+/-22 mmHg. SP: 114+/-25 mmHg. ISP: 109+/-26 mmHg. DP: 67+/-23 mmHg. IDP: 66+/-22 mmHg. CVP: 5+/-3 mmHg. RR: 19+/-11 rpm. V(T): 14+/-7 ml/kg. V(M): 191+/-93 ml/kg/min. EtCO(2): 40+/-8 mmHg. T: 37.1+/-1.7 degrees C. ASA III and ASA IV patients, compared with those with ASA I, showed higher values of HR, RR, V(T) and V(M) and lower in IMAP, CVP, EtCO(2), SpO(2) and T. The most frequent complications were bradycardia (36.3% of the patients), hypotension (37.9%), hypoventilation (63.4%), hypoxia (16.4%), hypothermia (4.8%) and death (0.9%). Cardiorespiratory complications frequently occur in dogs during general anaesthesia.