Effect of maropitant,a neurokinin‐1 receptor antagonist,on the minimum alveolar concentration of sevoflurane during stimulation of the ovarian ligament in cats

ObjectiveDetermine if maropitant decreases the minimum alveolar concentration (MAC) of sevoflurane during stimulation of the ovarian ligament in cats.Study designProspective study.AnimalsFifteen, female cats weighing 2.5 ± 0.6kg (mean ± SD).MethodsAnesthesia was induced and maintained with sevoflurane. The right ovary was accessed via laparoscopy. A suture around the ovary and ovarian ligament was exteriorized through the abdominal wall for stimulation. A stimulus–response curve was created to identify the optimal force for MAC comparisons. In 10 cats, MAC was determined with only sevoflurane (baseline) then after 1 and 5 mg kg^?1 intravenous maropitant administration. The stimulation tension force used was 4.9 N. Repeated measures anova was used to compare the groups. MAC was defined as the average of the cross‐over concentrations and reported MAC is adjusted to sea‐level and depicted as mean ± SD.ResultsThe stimulus‐response curve was hyperbolic and plateaued at 4.3 ± 3 N. The optimal tension force chosen to compare MAC was 4.9 N. The baseline sevoflurane MAC was 2.96 ± 0.3%. Maropitant, 1 mg kg^?1, decreased the MAC to 2.51 ± 0.3% (15%, p < 0.01). The higher maropitant dose of 5 mg kg^?1 did not change MAC further when compared to the low dose (2.46 ± 0.4%, p = 0.33).Conclusion and clinical relevanceThe ovarian ligament stimulation model is suitable to determine MAC during visceral stimulation in cats. Maropitant decreased the anesthetic requirements during visceral ovarian and ovarian ligament stimulation in cats. Maropitant (1 mg kg^?1) decreases MAC by 15%; a higher dose had no additional effect.     

Combined effects of dexmedetomidine and vatinoxan infusions on minimum alveolar concentration and cardiopulmonary function in sevoflurane-anesthetized dogs

ObjectiveTo evaluate the effects of combined infusions of vatinoxan and dexmedetomidine on inhalant anesthetic requirement and cardiopulmonary function in dogs.Study designProspective experimental study.MethodsA total of six Beagle dogs were anesthetized to determine sevoflurane minimum alveolar concentration (MAC) prior to and after an intravenous (IV) dose (loading, then continuous infusion) of dexmedetomidine (4.5 μg kg^–1 hour^–1) and after two IV doses of vatinoxan in sequence (90 and 180 μg kg^–1 hour^–1). Blood was collected for plasma dexmedetomidine and vatinoxan concentrations. During a separate anesthesia, cardiac output (CO) was measured under equivalent MAC conditions of sevoflurane and dexmedetomidine, and then with each added dose of vatinoxan. For each treatment, cardiovascular variables were measured with spontaneous and controlled ventilation. Repeated measures analyses were performed for each response variable; for all analyses, p < 0.05 was considered significant.ResultsDexmedetomidine reduced sevoflurane MAC by 67% (0.64 ± 0.1%), mean ± standard deviation in dogs. The addition of vatinoxan attenuated this to 57% (0.81 ± 0.1%) and 43% (1.1 ± 0.1%) with low and high doses, respectively, and caused a reduction in plasma dexmedetomidine concentrations. Heart rate and CO decreased while systemic vascular resistance increased with dexmedetomidine regardless of ventilation mode. The co-administration of vatinoxan dose-dependently modified these effects such that cardiovascular variables approached baseline.Conclusions and clinical relevanceIV infusions of 90 and 180 μg kg^–1 hour^–1 of vatinoxan combined with 4.5 μg kg^–1 hour^–1 dexmedetomidine provide a meaningful reduction in sevoflurane requirement in dogs. Although sevoflurane MAC-sparing properties of dexmedetomidine in dogs are attenuated by vatinoxan, the cardiovascular function is improved. Doses of vatinoxan >180 μg kg^–1 hour^–1 might improve cardiovascular function further in combination with this dose of dexmedetomidine, but beneficial effects on anesthesia plane and recovery quality may be lost.     

Effects of continuous intravenous infusion of morphine and morphine‐tramadol on the minimum alveolar concentration of sevoflurane and electroencephalographic entropy indices in dogs

ObjectiveTo compare the effects of continuous rate infusions (CRIs) of intravenous (IV) morphine and morphine-tramadol on the minimum alveolar concentration (MAC) of sevoflurane, and on electroencephalographic entropy indices in dogs.DesignProspective study.AnimalsEight young, healthy German shepherds, weighing 26.3 ± 3.1 kg (mean ± SD).MethodsAnaesthesia was induced and maintained with sevoflurane. A standard tail-clamp technique was used for MAC determination. Within one anaesthetic period, MAC was first determined during sevoflurane anaesthesia alone (MAC_B); then during morphine infusion (MAC_M), (loading dose 0.5 mg kg⁻¹IM; CRI, 0.2 mg kg⁻¹hour⁻¹⁾ then finally during morphine-tramadol infusion (tramadol loading dose 1.5 mg kg⁻¹IV; CRI, 2.6 mg kg⁻¹ hour⁻¹) (MAC_MT). At each change, periods of 45 minutes were allowed for equilibration. Stated entropy (SE), response entropy (RE), and RE-SE differences were measured five minutes prior to and during tail clamping.ResultsThe MAC_B was 2.1 ± 0.3vol%. The morphine and morphine-tramadol infusions reduced MAC to 1.6 ± 0.3vol% and 1.3 ± 0.3vol%, respectively. MAC was decreased below baseline more during morphine-tramadol than during morphine alone (39 ± 9% versus 25 ± 6%, respectively; p = 0.003). All SE and RE and most RE-SE differences were increased significantly (p < 0.05) over pre-stimulation in all groups when the dogs responded purposefully to noxious stimulation. When no response to noxious stimulation occurred, the entropy indices did not change.Conclusion and clinical relevanceIn dogs, combined morphine-tramadol CRI decreased sevoflurane MAC more than morphine CRI alone. Entropy indices changed during nociceptive responses in anaesthetized animals, suggesting that entropy measurements may be useful in determining anaesthetic depth in dogs.     

Effects of tramadol on the minimum alveolar concentration of sevoflurane in dogs

ObjectiveTo evaluate the effect of tramadol on sevoflurane minimum alveolar concentration (MAC_SEVO) in dogs. It was hypothesized that tramadol would dose-dependently decrease MAC_SEVO.Study designRandomized crossover experimental study.AnimalsSix healthy, adult female mixed-breed dogs (24.2 ± 2.6 kg).MethodsEach dog was studied on two occasions with a 7-day washout period. Anesthesia was induced using sevoflurane delivered via a mask. Baseline MAC (MAC_B) was determined starting 45 minutes after tracheal intubation. A noxious stimulus (50 V, 50 Hz, 10 ms) was applied subcutaneously over the mid-humeral area. If purposeful movement occurred, the end-tidal sevoflurane was increased by 0.1%; otherwise, it was decreased by 0.1%, and the stimulus was re-applied after a 20-minute equilibration. After MAC_B determination, dogs randomly received a tramadol loading dose of either 1.5 mg kg^?1 followed by a continuous rate infusion (CRI) of 1.3 mg kg^?1 hour^?1 (T1) or 3 mg kg^?1 followed by a 2.6 mg kg^?1 hour^?1 CRI (T2). Post-treatment MAC determination (MAC_T) began 45 minutes after starting the CRI. Data were analyzed using a mixed model anova to determine the effect of treatment on percentage change in baseline MAC_SEVO (p < 0.05).ResultsThe MAC_B values were 1.80 ± 0.3 and 1.75 ± 0.2 for T1 and T2, respectively, and did not differ significantly. MAC_T decreased by 26 ± 8% for T1 and 36 ± 12% for T2. However, there was no statistically significant difference in the decrease between the two treatments.Conclusion and clinical relevanceTramadol significantly reduced MAC_SEVO but this was not dose dependent at the doses studied.     

Determination of the sevoflurane sparing effect of methadone in cats

ObjectiveTo determine the magnitude and duration of sevoflurane minimum alveolar concentration (MAC) reduction following a single intravenous (IV) dose of methadone in cats.Study designProspective experimental study.AnimalsEight (four females and four males) healthy mixed-breed adult (1–2 years) cats weighing 5.82 ± 0.42 kg.MethodsAnesthesia was induced and maintained with sevoflurane. Intravenous catheters facilitated administration of methadone and lactated Ringer’s solution. After baseline MAC determination in triplicate using a tail clamp technique, 0.3 mg kg^?1 of methadone was administered IV. End-tidal sevoflurane concentration (e′SEVO) was reduced and MAC was redetermined. In an effort to determine the duration of MAC reduction, measurements were repeated in a stepwise manner until MAC values returned to baseline. After the last stimulation, the e′SEVO was increased to 1.2 individual MAC for 15 minutes, then sevoflurane was discontinued and cats were allowed to recover from anesthesia.ResultsBaseline sevoflurane MAC was 3.18 ± 0.06%. When compared with baseline the sevoflurane MAC after methadone administration was significantly reduced by 25, 15 and 7% at 26, 76 and 122 minutes, respectively. The final MAC value (3.09 ± 0.07%) determined 156 minutes after methadone administration was not significantly different from baseline.Conclusions and clinical relevanceIntravenous methadone (0.3 mg kg^?1) significantly decreased MAC of sevoflurane in cats but the effect was short-lived.     

Evaluation of analgesic and physiologic effects of epidural morphine administered at a thoracic or lumbar level in dogs undergoing thoracotomy

ObjectiveTo evaluate the analgesic and physiological effects of epidural morphine administered at the sixth and seventh lumbar or the fifth and sixth thoracic vertebrae in dogs undergoing thoracotomy.Study designProspective, randomized, blinded trial.AnimalsFourteen mixed-breed dogs, weighing 8.6 ± 1.4 kg.MethodsThe animals received acepromazine (0.1 mg kg^?1) IM and anesthesia was induced with propofol (4 mg kg^?1) IV. The lumbosacral space was punctured and an epidural catheter was inserted up to the region between the sixth and seventh lumbar vertebrae (L, n = 6) or up to the fifth or sixth intercostal space (T, n = 8). The dogs were allowed to recover and after radiographic confirmation of correct catheter position, anesthesia was reinduced with propofol IV and maintained with 1.7% isoflurane. Following stabilization of monitored parameters, animals received morphine (0.1 mg kg^?1) diluted in 0.9% NaCl to a final volume of 0.25 mL kg^?1 via the epidural catheter, and after 40 minutes, thoracotomy was initiated. Heart rate and rhythm, systolic, mean and diastolic arterial pressures, respiratory rate, arterial hemoglobin oxygen saturation, partial pressure of expired CO₂ and body temperature were measured immediately before the epidural administration of morphine (0 minute) and every 10 minutes during the anesthetic period. The Melbourne pain scale and the visual analog scale were used to assess post-operative pain. The evaluation began 3 hours after the epidural administration of morphine and occurred each hour until rescue analgesia.ResultsThere were no important variations in the physiological parameters during the anesthetic period. The post-operative analgesic period differed between the groups, being longer in T (9.9 ± 1.6 hours) compared with L (5.8 ± 0.8 hours).ConclusionsThe use of morphine, at a volume of 0.25 mL kg^?1, administered epidurally over the thoracic vertebrae provided longer lasting analgesia than when deposited over the lumbar vertebrae.Clinical relevanceThe deposition of epidural morphine provided longer lasting analgesia when administered near to the innervation of the injured tissue without increasing side effects.     

Cardiopulmonary effects of butorphanol in sevoflurane‐anesthetized guineafowl (Numida meleagris)

ObjectiveTo evaluate the cardiopulmonary changes induced by intravenous butorphanol administration in guineafowl anesthetized with sevoflurane.Study designProspective experimental trial.AnimalsEight adult guineafowl (Numida meleagris) weighing 1.61 ± 0.49 kg were used for the study.MethodsBirds were anesthetized with sevoflurane and allowed to breathe spontaneously. After endotracheal intubation, end-tidal sevoflurane was adjusted to 1.0 individual sevoflurane MAC that was previously determined in triplicate using a standard bracketing technique. The brachial artery was catheterized for direct pressure measurement and blood sampling. Heart rate and rhythm were monitored by electrocardiography and respiratory rate was recorded. Baseline data were recorded 30 minutes after induction. Then, end-tidal sevoflurane was adjusted to 0.8 individual MAC and after 15 minutes physiologic variables were measured again. Subsequently, butorphanol (4 mg kg^?1) was administered intravenously over 10 seconds and physiologic responses were recorded at 1, 5, 10, 15, 20, 30 and 45 minutes after administration.ResultsButorphanol administration was associated with arrhythmias in all birds, including second-degree atrioventricular block, sinus arrest, ventricular and supraventricular tachycardia and ventricular premature complexes. Heart rate and arterial blood pressures decreased significantly 1 minute after butorphanol administration. Two birds developed severe hypotension, apnea and ventricular fibrillation 5 minutes after administration, and one died.Conclusions and clinical relevanceThe butorphanol dose (4 mg kg^?1) that produces clinically relevant sevoflurane MAC reduction in guineafowl caused severe adverse cardiopulmonary effects in two birds and was considered unsafe under the conditions used in this study.     

Ketoprofen reduces the minimum alveolar concentration (MAC) in dogs anaesthetized with isoflurane and fentanyl

Non‐steroidal anti‐inflammatory drugs may potentiate the opioid induced reduction in volatile anaesthetic requirements ( Gomez de Segura et al. 1998 ). This study determined the reduction in the MAC of isoflurane (ISO) produced by ketoprofen (KETO) in dogs anaesthetized with fentanyl (FENT) and ISO. Six healthy female crossbred dogs, weighing 13.5 ± 1.3 (mean ± SD) kg and aged 3.0 ± 0.9 years were studied. Approval of the study was obtained from the institutional ethics committee. Anaesthesia was induced in all dogs via a facemask with 5% ISO in 5 L minute^?1 oxygen. The dogs' trachea were intubated and lungs were ventilated to maintain normocapnia (Pe ′CO₂ 4.7–6 kPa, 35–45 mm Hg). A heating pad was used to maintain body temperature. The animals were anaesthetized four times at one week intervals with the following anaesthetic and analgesic protocols randomly administered. Study 1, MAC (ISO); Isoflurane MAC. Study 2, MAC (ISO + FENT); dogs anaesthetized with ISO received a loading dose of 30 µg kg^?1 FENT IV over 20 minutes followed by a maintenance infusion of 0.2 µg kg^?1 minute^?1 FENT. Study 3, MAC (ISO + FENT + KETO1); as study 2 plus 1 mg kg^?1 KETO. Study 4, MAC (ISO + FENT + KETO2); as study 2 plus 2 mg kg^?1 KETO. The MAC was determined in duplicate by applying a standard electrical stimulus (50 V, 50 H₂ over 60 seconds via two needles placed SC over the tarsus). The stimulus was applied 15 minutes after every step change in anesthetic concentration. The Wilcoxon test was applied to data to determine significant differences among MAC measurements. Fentanyl significantly decreased MAC (ISO) from 1.27% ± 0.02% to 0.73% ± 0.08%, a reduction of 42% (p < 0.05). Ketoprofen 1 mg kg^?1 further decreased the MAC value (although not statistically significantly) with a reduction of 47% from MAC (ISO) (0.67% ± 0.13%) and 8% from MAC (ISO + FENT). When KETO 2 mg kg^?1 was given, the reduction in MAC was 50% compared to MAC (ISO) (0.63% ± 0.08%; p < 0.05) and 14% compared to MAC (ISO + FENT) p < 0.05. Administration of KETO further reduces MAC (ISO) compared to levels observed with FENT alone. The observed reduction may have clinical advantages.     

Maropitant prevented vomiting but not gastroesophageal reflux in anesthetized dogs premedicated with acepromazine‐hydromorphone

ObjectiveTo evaluate the efficacy of maropitant for prevention of vomiting and gastroesophageal reflux (GER) in dogs following acepromazine-hydromorphone premedication and inhalation anesthesia.Study designRandomized, blinded, prospective clinical study.AnimalsTwenty-six dogs admitted for elective soft tissue or orthopedic procedures that were 3.1 ±3.1 years of age and weighed 20.5 ± 11.4 kg.MethodsDogs were randomly assigned to one of two groups: Group M received maropitant (1.0 mg kg^?1) and Group S received 0.9% saline (0.1 mL kg^?1) intravenously 45–60 minutes before premedication with hydromorphone (0.1 mg kg^?1) and acepromazine (0.03 mg kg^?1) intramuscularly. An observer blinded to treatment documented any retching or vomiting for 20 minutes before induction with propofol (2–6 mg kg^?1) and inhalation anesthesia. A pH probe inserted into the distal esophagus was used to detect GER.ResultsNone of the dogs in Group M retched or vomited (0/13), 6/13 (46%) in Group S were observed to retch or vomit, and the difference between groups was significant (p = 0.015). There were no differences between groups in the number of dogs with GER (Group M: 4/13, Group S: 6/13 dogs) or the number of reflux events. Esophageal pH at the end of anesthesia was significantly lower in both M and S groups in dogs with GER versus dogs without GER (p = 0.004 and 0.011, respectively). Only dogs with GER in Group S had significantly lower pH at the end compared to the beginning of anesthesia (p = 0.004).Conclusions and clinical relevanceIntravenous maropitant prevented retching and vomiting associated with acepromazine-hydromorphone premedication. Maropitant did not prevent the occurrence of GER. Fewer dogs in Group M developed GER but further study with a larger number of dogs is necessary to determine if there is a significant difference.     

Effects of constant rate infusions of dexmedetomidine or MK-467 on the minimum alveolar concentration of sevoflurane in dogs

Objective

To determine the effects of low and high dose infusions of dexmedetomidine and a peripheral α₂-adrenoceptor antagonist, MK-467, on sevoflurane minimum alveolar concentration (MAC) in dogs.

The effect of experimentally induced hypothyroidism on the isoflurane minimum alveolar concentration in dogs

ObjectiveTo determine the effect of experimentally induced hypothyroidism on isoflurane (ISO) minimum alveolar concentration (MAC) in dogs.Study designProspective experimental study.AnimalsEighteen adult female mongrel dogs, age 2–4 years and weighing 8.2–13.1 kg.MethodsHypothyroidism was induced in nine dogs by the intravenous administration of 1 mCi kg⁻¹ of ¹³¹Iodine. The remaining nine dogs served as controls. Dogs were studied 9–12 months after the induction of hypothyroidism. Anesthesia was induced with ISO in oxygen via a mask. The trachea was intubated, and anesthesia was maintained using ISO in oxygen using a semi-closed rebreathing circle system. The dogs were mechanically ventilated to maintain an end-tidal carbon dioxide concentration between 35 and 45 mmHg. End-tidal ISO concentrations were measured with an infrared gas analyzer. The MAC was determined in duplicate using a tail clamp technique. The mean values for the groups were compared using a two sample t-test.ResultsThe mean ± SD MAC of isoflurane in the hypothyroid and euthyroid dogs was 0.98 ± 0.31% and 1.11 ± 0.26%, respectively. The mean MAC of isoflurane in hypothyroid dogs was not significantly different from the mean MAC of isoflurane in the control dogs (p=0.3553).Conclusion and clinical relevanceThe MAC of ISO in dogs was not significantly affected by experimentally induced hypothyroidism. The dose of ISO in dogs with hypothyroidism does not need to be altered.     

Effects of constant rate infusions of dexmedetomidine,remifentanil and their combination on minimum alveolar concentration of sevoflurane in dogs

ObjectiveTo evaluate the effects of constant rate infusions (CRIs) of dexmedetomidine and remifentanil alone and their combination on minimum alveolar concentration (MAC) of sevoflurane in dogs.Study designRandomized crossover experimental study.AnimalsA total of six (three males, three females) healthy, adult neutered Beagle dogs weighing 12.6 ± 1.4 kg.MethodsAnesthesia was induced with sevoflurane in oxygen until endotracheal intubation was possible and anesthesia maintained with sevoflurane using positive-pressure ventilation. Each dog was anesthetized five times and was administered each of the following treatments: saline (1 mL kg^–1 hour^–1) or dexmedetomidine at 0.1, 0.5, 1.0 or 5.0 μg kg^–1 loading dose intravenously over 10 minutes followed by CRI at 0.1, 0.5, 1.0 or 5.0 μg kg^–1 hour^–1, respectively. Following 60 minutes of CRI, sevoflurane MAC was determined in duplicate using an electrical stimulus (50 V, 50 Hz, 10 ms). Then, CRI of successively increasing doses of remifentanil (0.15, 0.60 and 2.40 μg kg^–1 minute^–1) was added to each treatment. MAC was also determined after 30 minutes equilibration at each remifentanil dose. Isobolographic analysis determined interaction from the predicted doses required for a 50% MAC reduction (ED₅₀) with remifentanil, dexmedetomidine and remifentanil combined with dexmedetomidine, with the exception of dexmedetomidine 5.0 μg kg^–1 hour^–1, obtained using log-linear regression analysis.ResultsThe sevoflurane MAC decreased dose-dependently with increasing infusion rates of dexmedetomidine and remifentanil. Remifentanil ED₅₀ values were lower when combined with dexmedetomidine than those obtained during saline–remifentanil. Synergistic interactions between dexmedetomidine and remifentanil for MAC reduction occurred with dexmedetomidine at 0.5 and 1.0 μg kg^–1 hour^–1.Conclusions and clinical relevanceCombined CRIs of dexmedetomidine and remifentanil synergistically resulted in sevoflurane MAC reduction. The combination of dexmedetomidine and remifentanil effectively reduced the requirement of sevoflurane during anesthesia in dogs.     

Effect of oral trazodone on the minimum alveolar concentration of isoflurane in dogs

Objective

To determine the effect of oral trazodone on the minimum alveolar concentration (MAC) of isoflurane in dogs.

Cardiovascular effects of epidural administration of methadone, ropivacaine 0.75% and their combination in isoflurane anaesthetized dogs

ObjectiveTo compare the cardiovascular effects of four epidural treatments in isoflurane anaesthetised dogs.Study designProspective, randomized. experimental study.AnimalsSix female, neutered Beagle dogs (13.3 ± 1.0 kg), aged 3.6 ± 0.1 years.MethodsAnaesthesia was induced with propofol (8.3 ± 1.1 mg kg^?1) and maintained with isoflurane in a mixture of oxygen and air [inspiratory fraction of oxygen (FiO₂) = 40%], using intermittent positive pressure ventilation. Using a cross-over model, NaCl 0.9% (P); methadone 1% 0.1 mg kg^?1 (M); ropivacaine 0.75% 1.65 mg kg^?1 (R) or methadone 1% 0.1 mg kg^?1 + ropivacaine 0.75% 1.65 mg kg^?1 (RM) in equal volumes (0.23 mL kg^?1) using NaCl 0.9%, was administered epidurally at the level of the lumbosacral space. Treatment P was administered to five dogs only. Cardiovascular and respiratory variables, blood gases, and oesophageal temperature were recorded at T-15 and for 60 minutes after epidural injection (T0).ResultsMean overall heart rate (HR in beats minute^?1) was significantly lower after treatment M (119 ± 16) (p = 0.0019), R (110 ± 18) (p < 0.0001) and RM (109 ± 13) (p < 0.0001), compared to treatment P (135 ± 21). Additionally, a significant difference in HR between treatments RM and M was found (p = 0.04). After both ropivacaine treatments, systemic arterial pressures (sAP) were significantly lower compared to other treatments. No significant overall differences between treatments were present for central venous pressure, cardiac output, stroke volume, systemic vascular resistance, oxygen delivery and arterial oxygen content (CaO₂). Heart rate and sAP significantly increased after treatment P and M compared to baseline (T-15). With all treatments significant reductions from baseline were observed in oesophageal temperature, packed cell volume and CaO₂. A transient unilateral Horner’s syndrome occurred in one dog after treatment R.Conclusions and clinical relevanceClinically important low sAPs were observed after the ropivacaine epidural treatments in isoflurane anaesthetised dogs. Systemic arterial pressures were clinically acceptable when using epidural methadone.     

The use of pulsed electromagnetic field (PEMF) therapy to provide post-operative analgesia in the dog

Buprenorphine is an effective analgesic when administered epidurally to humans. The purpose of this study was to compare epidural buprenorphine (B; n = 10) with epidural morphine (M; n = 10) for post‐operative analgesia in dogs undergoing cranial cruciate ligament repair. All dogs were premedicated with acepromazine (0.1 mg kg^?1 IM), induced with propofol (4–6 mg kg^?1 IV) and maintained with halothane in oxygen. Dogs were randomly assigned to receive B (0.004 mg kg^?1) or M (0.1 mg kg^?1) in the lumbosacral epidural space in a total volume of 0.2 mL kg^?1. End‐tidal halothane and CO₂ and temperature were recorded every 15 minutes until extubation (t = 0). A numerical rating pain score (SPS) was recorded at t = 0, 1, 2, 4, 6, 10 and 24 hours by a blinded observer. Dogs received rescue morphine (1.0 mg kg^?1 IM) if indicated by SPS and the time of rescue analgesic administration was recorded. Observable side‐effects such as urinary retention, sedation or pruritus were recorded. Data were analyzed with repeated measures anova . Mean ± SD body weight (kg) and age (yrs) for B dogs was 34.2 ± 10.8 and 5.5 ± 2.8; for M dogs these values were 36.6 ± 13.5 and 5.9 ± 3.3. Mean ± SD SPS for B dogs at t = 0, 1, 2, 4, 6, 10 and 24 hours were 1.2 ± 0.75, 3.2 ± 2.0, 4.5 ± 4.3, 4.6 ± 3.4, 4.7 ± 3.0, 5.0 ± 4.9 and 5.1 ± 3.5. For M dogs these values were 1.7 ± 0.5, 2.6 ± 2.0, 3.7 ± 0.75, 4.2 ± 2.2, 4.1 ± 3.0, 3.1 ± 2.1 and 3.9 ± 1.9. There were no significant differences between B and M with respect to SPS, times or frequency of rescue morphine administration, end‐tidal halothane and CO₂, or esophageal temperature. Fifty per cent of dogs in both groups required rescue morphine. Buprenorphine is as effective as morphine for epidural analgesia in healthy dogs undergoing hindlimb orthopedic surgery.     

Caudal epidural anti‐nociception using lidocaine,bupivacaine or their combination in cows undergoing reproductive procedures

ObjectiveTo evaluate the anti-nociceptive effects of lidocaine, lidocaine-bupivacaine combination or bupivacaine following caudal epidural administration in cows undergoing reproductive procedures.Study designBlinded, randomized experimental study.AnimalsThirty seven healthy Holstein cows (mean weight ± SD, 633 ± 41 kg).MethodsAnimals were allocated randomly to receive one of four treatments: group LID, 0.2 mg kg^?1 lidocaine 2%; group LID-BUP, lidocaine-bupivacaine mixture in a 1:1 volume ratio (0.1 mg kg^?1 and 0.025 mg kg^?1, respectively); group BUP-LD, 0.05 mg kg^?1 bupivacaine 0.5%; and group BUP-HD, 0.06 mg kg^?1 bupivacaine 0.5%. The onset and duration of perineal anti-nociception were determined using superficial and deep pin pricks and the number of cows with complete perineal anti-nociception was recorded. Parameters were compared using anova followed by Duncan's test where relevant.ResultsMean ± SD time to onset of anti-nociception following epidural administration of BUP-LD was significantly longer than for LID-BUP (p < 0.05). The duration (in minutes) of perineal anti-nociception was significantly longer following epidural administration of BUP-HD (247 ± 31) versus LID-BUP (181 ± 33) and LID (127 ± 25) minutes respectively. The % of cows with complete anti-nociception was increased in the group treated with BUP-HD compared to BUP-LD. Severe ataxia or recumbency did not occur in any groups.Conclusions and clinical relevanceEpidurally administered bupivacaine, at a dose of 0.06 mg kg^?1, may provide satisfactory caudal epidural anti-nociception for longer-duration obstetric and surgical procedures.     

Influence of a preload of hydroxyethylstarch 6% on the cardiovascular effects of epidural administration of ropivacaine 0.75% in anaesthetized dogs

ObjectiveTo evaluate the cardiovascular effects of a preload of hydroxyethylstarch 6% (HES), preceding an epidural administration of ropivacaine 0.75% in isoflurane anaesthetized dogs.AnimalsSix female, neutered Beagle dogs (mean 13.3 ± SD 1.0 kg; 3.6 ± 0.1 years).Study designRandomized experimental cross-over study (washout of 1 month).MethodsAnaesthesia was induced with propofol and maintained with isoflurane in oxygen/air. All dogs were anaesthetized twice to receive either treatment HESR (continuous rate infusion [CRI] of 7 mL kg^?1 HES started 30 minutes [T-30] prior to epidural administration of ropivacaine 0.75% 1.65 mg kg^?1 at T0) or treatment R (no HES preload and similar dose and timing of epidural ropivacaine administration). Baseline measurements were obtained at T-5. Heart rate (HR), mean (MAP), diastolic (DAP) and systolic (SAP) invasive arterial pressures, cardiac output (Lithium dilution and pulse contour analysis) and derived parameters were recorded every 5 minutes for 60 minutes. Statistical analysis was performed on five dogs, due to the death of one dog.ResultsClinically relevant decreases in MAP (<60 mmHg) were observed for 20 and 40 minutes following epidural administration in treatments HESR and R respectively. Significant decreases in MAP and DAP were present after treatment HESR for up to 20 minutes following epidural administration. No significant within-treatment and overall differences were observed for other cardiovascular parameters. A transient unilateral Horner's syndrome occurred in two dogs (one in each treatment). One dog died after severe hypotension, associated with epidural anaesthesia.Conclusions and clinical relevanceA CRI of 7 mL kg^?1 HES administered over 30 minutes before epidural treatment did not prevent hypotension induced by epidural ropivacaine 0.75%. Epidural administration of ropivacaine 0.75% in isoflurane anaesthetized dogs was associated with a high incidence of adverse effects in this study.     

A comparison of epidural analgesia provided by bupivacaine alone,bupivacaine + morphine,or bupivacaine + dexmedetomidine for pelvic orthopedic surgery in dogs

ObjectiveTo compare the analgesic efficacy of bupivacaine, bupivacaine + morphine, or bupivacaine + dexmedetomidine administered epidurally in dogs undergoing pelvic limb orthopedic surgery.Study designProspective, randomized, double blinded clinical trial.AnimalsSixty dogs weighing (mean ± SD) 35 ± 15.7 kg, aged 5 ± 3 years.MethodsDogs were assigned to receive a lumbosacral epidural containing bupivacaine (B) 0.5%, 1 mg kg^?1; B, bupivacaine 0.5%, 1 mg kg^?1 + morphine 1%, 0.1 mg kg^?1; B + M, or bupivacaine 0.5%, 1 mg kg^?1 + dexmedetomidine 0.05%, 4 μg kg^?1; B + D. The anesthetic protocol was standardized. The median expired isoflurane concentration (E′Iso) and requirement for additional induction agent preventing purposeful movement were recorded. Pain was scored using visual analog (VAS) and modified University of Melbourne (UMPS) pain scales. Sedation was assessed using a 0–4 scale. All parameters were recorded preoperatively, and at extubation (t = 0), then at 1, 2, 4, 8, 12, 16, and 20–24 hours. Hydromorphone was administered postoperatively to patients with a VAS ≥ 35 and/or UMPS ≥ 9. Time to first voluntary urination and first motor activity were recorded.ResultsPostoperatively, B + D had a lower UMPS pain score than B at t = 1 hour (p = 0.013), but not compared to B + M. The B + D group had a shorter time to urination (p = 0.0131) and a longer time for return of motor function (p = 0.0068). There were no other differences between the treatments.Conclusion and clinical relevanceEpidurally administered B, B + M, or B + D in dogs all provided acceptable analgesia to manage post–operative orthopedic pelvic limb pain. Epidural administration of B + D is an effective alternative to the analgesia provided by B or B + M, but is associated with increased time to return of motor function. The direct neurotoxic effects of epidural dexmedetomidine have not been fully tested.     

Effects of pre‐operative administration of medetomidine on plasma insulin and glucose concentrations in healthy dogs and dogs with insulinoma

ObjectiveTo investigate the effect of medetomidine on plasma glucose and insulin concentrations in dogs with insulinoma and in healthy dogs undergoing anesthesia and surgery.AnimalsTwenty–five dogs with insulinoma and 26 healthy dogs.MethodsIn dogs with insulinoma, medetomidine (5 μg kg^?1) was randomly included (n = 12) or omitted (n = 13) from the pre–anesthetic medication protocol, which typically contained an opioid and an anticholinergic. Healthy dogs received medetomidine (5 μg kg^?1; n = 13) or acepromazine (0.04 mg kg^?1; n = 13) plus an opioid (morphine 0.5 mg kg^?1) and an anticholinergic (atropine 0.04 mg kg^?1) as pre–anesthetic medications. Pre–anesthetic medications were given intramuscularly. Plasma glucose and insulin concentrations were measured before (sample 1) and 30 minutes after pre–anesthetic medication (sample 2), and at the end of surgery in dogs with insulinoma or at 2 hours of anesthesia in healthy dogs (sample 3). Glucose requirement to maintain intra–operative normoglycemia in dogs with insulinoma was quantified and compared. Data were analyzed with anova and Bonferroni post–test, t–tests or chi–square tests as appropriate with p < 0.05 considered significant. Data are shown as mean ± SD.ResultsMedetomidine significantly decreased plasma insulin concentrations and increased plasma glucose concentrations in healthy dogs and those with insulinoma. These variables did not change significantly in the dogs not receiving medetomidine. In the dogs with insulinoma, intra–operative glucose administration rate was significantly less in the animals that received medetomidine compared to those that did not.ConclusionsPre–anesthetic administration of medetomidine significantly suppressed insulin secretion and increased plasma glucose concentration in dogs with insulinoma and in healthy dogs undergoing anesthesia and surgery.Clinical relevanceThese findings support the judicious use of medetomidine at low doses as an adjunct to the anesthetic management of dogs with insulinoma.     

GABA(A) receptor antagonism increases NMDA receptor inhibition by isoflurane at a minimum alveolar concentration

ObjectiveAt the minimum alveolar concentration (MAC), isoflurane potentiates GABA_A receptor currents and inhibits NMDA receptor currents, and these actions may be important for producing anesthesia. However, isoflurane modulates GABA_A receptors more potently than NMDA receptors. The objective of this study was to test whether isoflurane would function as a more potent NMDA receptor antagonist if its efficacy at GABA_A receptors was decreased.Study designProspective experimental study.AnimalsFourteen 10-week-old male Sprague–Dawley rats weighing 269 ± 12 g.MethodsIndwelling lumbar subarachnoid catheters were surgically placed in isoflurane-anesthetized rats. Two days later, the rats were anesthetized with isoflurane, and artificial CSF containing either 0 or 1 mg kg^?1 picrotoxin, a GABA_A receptor antagonist, was infused intrathecally at 1 μL minute^?1. The baseline isoflurane MAC was then determined using a standard tail clamp technique. MK801 (dizocilpine), an NMDA receptor antagonist, was then administered intravenously at 0.5 mg kg^?1. Isoflurane MAC was re-measured.ResultsPicrotoxin increased isoflurane MAC by 16% compared to controls. MK801 significantly decreased isoflurane MAC by 0.72% of an atmosphere in controls versus 0.47% of an atmosphere in rats receiving intrathecal picrotoxin.Conclusions and clinical relevanceA smaller MK801 MAC-sparing effect in the picrotoxin group is consistent with greater NMDA antagonism by isoflurane in these animals, since it suggests that fewer NMDA receptors are available upon which MK801 could act to decrease isoflurane MAC. Decreasing isoflurane GABA_A potentiation increases isoflurane NMDA antagonism at MAC. Hence, the magnitude of an anesthetic effect on a given channel or receptor at MAC may depend upon effects at other receptors.