To compare the duration of bupivacaine liposome suspension in the dog with that of bupivacaine and dexmedetomidine following a perineural injection.
8 healthy Beagles.
The left sciatic nerve of each dog was randomly assigned to an ultrasound-guided perineural injection with either bupivacaine liposome suspension (BLS) or with 0.5% bupivacaine with dexmedetomidine (1 µg/mL) (BUP-DEX). The contralateral nerve was assigned to the alternate agent. The sensory, motor, and proprioceptive functions were evaluated before the injection (baseline) and at 4, 10, 24, 48, 72, and 96 hours.
The block in 1 limb in the BLS treatment appeared to have failed (data set excluded). The motor scores of 2 individuals could not be evaluated leaving 5 limbs to evaluate in the BLS treatment and 6 in the BUP-DEX.
A total of 6 out of 7 limbs in the BLS achieved a complete sensory block. In 3 out of 5 treatments with BLS, motor block was only partial and in 2 not apparent at all. Proprioceptive block was partial in 5 out of 7 dogs in the BLS treatment. All functions were still completely obliterated at 10 hours in 6 cases in treatment BUP-DEX. All functions were restored in all cases by 96 and 24 hours after administration of BLS and BUP-DEX, respectively.
The blockade characteristics of bupivacaine liposome suspension were effective and long lasting. Motor and proprioceptive deficits may be inconsistent over time.
To investigate use of a candidate maxillary nerve block in rabbits.
13 healthy New Zealand White rabbits (Oryctolagus cuniculus).
In phase 1, the maxillary nerve block procedure was performed in 7 sedated rabbits with 2 volumes (0.25 and 0.5 mL) of a saline (0.9% NaCl)-tissue marker dye solution (1 injection/side by random assignment). Rabbits were euthanized and dissected; numeric scales were used to rate injection accuracy and extent of staining. In phase 2, the nerve block was performed with articaine hydrochloride-epinephrine solution (0.5 mL) on a randomly assigned side in 6 sedated rabbits, with the contralateral side used as a control. Sensory function of the relevant dermatome was tested in triplicate with an algesiometer 0, 30, and 90 minutes after recovery from sedation. Statistical methods were used to compare results between injection volumes (phase 1) and between treated and control sides (phase 2).
In phase 1, dye was in contact with the targeted nerve after 13 of 14 injections. Accuracy and extent of staining did not differ significantly between volumes. In phase 2, algesiometer-applied force tolerance differed significantly between treated and control sides 30 minutes after recovery from sedation (56 to 145 minutes after the nerve block procedure). No adverse effects were detected in either study phase.
CONCLUSIONS AND CLINICAL RELEVANCE
The described technique for a maxillary nerve block was accurate and effective for desensitization of the relevant dermatome as assessed by algesiometry in healthy rabbits. Additional studies are needed to assess use of this procedure in rabbits of other breeds and its efficacy for clinical use. (Am J Vet Res 2020;81:843-848)
OBJECTIVE To evaluate the potency of vecuronium and duration of vecuronium-induced neuromuscular blockade in dogs with centronuclear myopathy (CNM).
ANIMALS 6 Labrador Retrievers with autosomal-recessive CNM and 5 age- and weight-matched control dogs.
PROCEDURES Dogs were anesthetized on 2 occasions (1-week interval) with propofol, dexmedetomidine, and isoflurane. Neuromuscular function was monitored with acceleromyography and train-of-four (TOF) stimulation. In an initial experiment, potency of vecuronium was evaluated by a cumulative-dose method, where 2 submaximal doses of vecuronium (10 μg/kg each) were administered IV sequentially. For the TOF's first twitch (T1), baseline twitch amplitude and maximal posttreatment depression of twitch amplitude were measured. In the second experiment, dogs received vecuronium (50 μg/kg, IV) and the time of spontaneous recovery to a TOF ratio (ie, amplitude of TOF's fourth twitch divided by amplitude of T1) ≥ 0.9 and recovery index (interval between return of T1 amplitude to 25% and 75% of baseline) were measured.
RESULTS Depression of T1 after each submaximal dose of vecuronium was not different between groups. Median time to a TOF ratio ≥ 0.9 was 76.7 minutes (interquartile range [IQR; 25th to 75th percentile], 66.7 to 99.4 minutes) for dogs with CNM and 75.0 minutes (IQR, 47.8 to 96.5 minutes) for controls. Median recovery index was 18.0 minutes (IQR, 9.7 to 23.5 minutes) for dogs with CNM and 20.2 minutes (IQR, 8 to 25.1 minutes) for controls.
CONCLUSIONS AND CLINICAL RELEVANCE For the study dogs, neither potency nor duration of vecuronium-induced neuromuscular blockade was altered by CNM. Vecuronium can be used to induce neuromuscular blockade in dogs with autosomal-recessive CNM.
To evaluate the cardiovascular effects of atipamezole administered at half the volume or the same volume as dexmedetomidine to isoflurane-anesthetized cats.
6 adult (1 to 2 years old) domestic shorthair cats (body weight, 3 to 6 kg).
Each cat was anesthetized with isoflurane and rocuronium 3 times; there was a 1-week washout period between successive anesthetic procedures. For each anesthetic procedure, dexmedetomidine (5 μg/kg) was administered IV. Five minutes after dexmedetomidine was administered, atipamezole (25 or 50 μg/kg) or saline (0.9% NaCl) solution was administered IM. Pulse rate, mean arterial blood pressure (MAP), cardiac output (CO), and systemic vascular resistance (SVR) were measured during anesthesia before dexmedetomidine administration (baseline), after dexmedetomidine administration, and 15, 30, 60, and 120 minutes after administration of atipamezole or saline solution. Pulse rate and MAP were also recorded when MAP was at its lowest value. Hemodynamic variables were compared among treatments at baseline, after dexmedetomidine administration, and after administration of atipamezole or saline solution. Effects of treatment and time on all variables were assessed with mixed-effects models.
Both doses of atipamezole resulted in a significantly lower MAP than did saline solution. Pulse rate, CO, and SVR were not significantly different among treatments after atipamezole or saline solution were administered.
CONCLUSIONS AND CLINICAL RELEVANCE
Atipamezole administered IM at half the volume or the same volume as dexmedetomidine was ineffective at increasing pulse rate or CO in anesthetized cats that received dexmedetomidine. However, atipamezole caused short-lasting but severe arterial hypotension.
PROCEDURES Cats were randomly assigned to receive maropitant (1 mg/kg [0.45 mg/lb], SC; maropitant group; n = 32) or saline (0.9% NaCl) solution (0.1 mL/kg [0.045 mL/lb], SC; control group; 34) 20 hours before IM administration of dexmedetomidine (20 μg/kg [9.1 μg/lb]) and morphine (0.1 mg/kg). Following administration of dexmedetomidine and morphine, the incidences of emesis, retching, and signs of nausea (sialorrhea and lip licking) were compared between the 2 groups. The aversive behavioral response of each cat to injection of maropitant or saline solution was scored on a visual analogue scale by each of 4 observers who were unaware of the treatment administered.
RESULTS Only 1 of 32 cats in the maropitant group vomited, whereas 20 of 34 control cats vomited. The incidences of emesis and retching for the maropitant group were significantly lower than those for the control group. The incidence of signs of nausea did not differ between the 2 groups. Visual analogue scale scores for the maropitant group were significantly higher than those for the control group.
CONCLUSIONS AND CLINICAL RELEVANCE Results of the present study indicated that administration of maropitant to healthy cats approximately 20 hours prior to administration of dexmedetomidine and morphine significantly decreased the incidence of emesis but did not decrease the incidence of signs of nausea. However, maropitant appeared to cause substantial discomfort when injected SC.
OBJECTIVE To evaluate potential associations between preanesthetic administration of acepromazine or dexmedetomidine and development of arterial hypotension or bradycardia in isoflurane-anesthetized dogs undergoing ovariohysterectomy.
ANIMALS 341 dogs.
PROCEDURES Medical records were searched to identify dogs that underwent ovariohysterectomy between January 2009 and December 2010 and received hydromorphone with acepromazine or dexmedetomidine as preanesthetic agents. Demographic data, sedative and anesthetic drugs, duration of anesthesia, average vaporizer setting, positive pressure ventilation, occurrence of hypotension (mean arterial pressure < 60 mm Hg) or bradycardia (> 50% reduction in heart rate, compared with the preanesthetic value), time to first occurrence and duration of hypotension, and treatment with dopamine or anticholinergic agents were recorded. Data were compared between dogs that received acepromazine and dexmedetomidine. Logistic regression was used to investigate associations between the treatments of interest (and other putative risk factors) and development of hypotension or bradycardia.
RESULTS For dogs that received acepromazine, the odds of developing hypotension were 2.61 times those for dogs that received dexmedetomidine. Hypotension occurred earlier and lasted longer in dogs that received acepromazine, and this group was treated with dopamine more frequently than the group that received dexmedetomidine. Lower body weight was associated with increased odds of hypotension. Odds of developing bradycardia were greater for dogs sedated with dexmedetomidine (vs acepromazine) and for dogs that underwent anesthetic induction with propofol or a ketamine-benzodiazepine combination (vs thiopental).
CONCLUSIONS AND CLINICAL RELEVANCE Anesthetic complications differed between isoflurane-anesthetized dogs undergoing ovariohysterectomy after premedication with acepromazine or dexmedetomidine in this study; future prospective investigations are warranted to investigate these effects in other, less homogenous populations of dogs.
Objective—To determine whether dogs that received eyedrops containing phenylephrine and scopolamine would have a higher mean arterial blood pressure (MAP) when anesthetized than would dogs that did not receive the eyedrops.
Animals—37 nondiabetic and 29 diabetic dogs anesthetized for phacoemulsification and 15 nondiabetic dogs anesthetized for corneal ulcer repair (control dogs).
Procedures—Medical records were reviewed to identify study dogs. Dogs undergoing phacoemulsification received 2 types of eyedrops (10% phenylephrine hydrochloride and 0.3% scopolamine hydrobromide) 4 times during a 2-hour period prior to the procedure. Control dogs did not receive these eyedrops. Heart rate and MAP were measured before surgery in all dogs 10 and 5 minutes before, at the time of (t0), and 5 (t5) and 10 (t10) minutes after atracurium administration.
Results—MAP was greater in the 2 groups that received the eyedrops than in the control group at t0 and t5; at t10, it was greater only for the nondiabetic dogs that received eyedrops. Nine nondiabetic dogs and 1 diabetic dog anesthetized for phacoemulsification had at least 1 MAP value > 131 mm Hg; 73% of MAP values > 131 mm Hg were detected within 10 minutes after atracurium administration. At no time did a control dog have an MAP value > 131 mm Hg.
Conclusions and Clinical Relevance—Anesthetized dogs pretreated with eyedrops containing phenylephrine and scopolamine had higher MAP values than dogs that did not receive the eyedrops, suggesting the drops caused hypertension. Atracurium may interact with the eyedrops and contribute to the hypertension.
OBJECTIVE To evaluate whether the ultrashort-acting neuromuscular blocking agent gantacurium can be used to blunt evoked laryngospasm in anesthetized cats and to determine the duration of apnea without hemoglobin desaturation.
ANIMALS 8 healthy adult domestic shorthair cats.
PROCEDURES Each cat was anesthetized with dexmedetomidine and propofol, instrumented with a laryngeal mask, and allowed to breathe spontaneously (fraction of inspired oxygen, 1.0). The larynx was stimulated by spraying sterile water (0.3 mL) at the rima glottidis; a fiberscope placed in the laryngeal mask airway was used to detect evoked laryngospasm. Laryngeal stimulation was performed at baseline; after IV administration of gantacurium at doses of 0.1, 0.3, and 0.5 mg/kg; and after the effects of the last dose of gantacurium had terminated. Duration of apnea and hemoglobin oxygen saturation (measured by means of pulse oximetry) after each laryngeal stimulation were recorded. Neuromuscular block was monitored throughout the experiment by means of acceleromyography on a pelvic limb.
RESULTS Laryngospasm was elicited in all cats at baseline, after administration of 0.1mg of gantacurium/kg, and after the effects of the last dose of gantacurium had terminated. The 0.3 and 0.5 mg/kg doses of gantacurium abolished laryngospasm in 3 and 8 cats, respectively, and induced complete neuromuscular block measured at the pelvic limb; the mean ± SE duration of apnea was 2 ± 1 minutes and 3 ± 1.5 minutes, respectively. Hemoglobin oxygen saturation did not decrease significantly after administration of any dose of gantacurium.
CONCLUSIONS AND CLINICAL RELEVANCE Gantacurium may reduce tracheal intubation-associated morbidity in cats breathing oxygen.
PROCEDURES Dogs were randomly assigned to receive either oxygen (Fio2 > 0.9 [100% oxygen]; n = 11; control group) or a mixture of nitrogen and oxygen (Fio2 = 0.4; 11; 40% oxygen group) as the carrier gas for isoflurane while anesthetized. All dogs were allowed to breathe spontaneously while anesthetized. For each dog, the Pao2, Paco2, other indices of oxygenation, and extent of sedation were monitored at predetermined times during and for 1 hour after anesthesia. Measured variables were compared between the 2 treatment groups and over time within each treatment group.
RESULTS None of the measured variables differed significantly between the control and 40% oxygen groups at any time during the postanesthesia period. Within each treatment group, the Paco2 and extent of sedation decreased over time during the postanesthesia period.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that indices of oxygenation did not differ significantly between healthy dogs in which the Fio2 was maintained at > 0.9 and those in which the Fio2 was maintained at 0.4 while anesthetized for ovariohysterectomy. Thus, the addition of nitrogen to the carrier gas for an inhalant anesthetic conferred neither an advantage nor disadvantage in regard to oxygenation during the first hour of anesthesia recovery.
OBJECTIVE To evaluate the efficacy of each of 3 incremental doses of MK-467 for alleviation of dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats.
ANIMALS 6 healthy adult domestic shorthair cats.
PROCEDURES Each cat was anesthetized with isoflurane and received a target-controlled infusion of dexmedetomidine estimated to maintain the plasma dexmedetomidine concentration at 10 ng/mL throughout the experiment. Heart rate (HR) and direct arterial pressures were measured at baseline (isoflurane administration only), during dexmedetomidine infusion, and before and after IV administration of each of 3 serially increasing doses (15, 30, and 60 μg/kg) of MK-467. Cardiac index (CI) and systemic vascular resistance (SVR) were recorded at baseline, during dexmedetomidine infusion, and at the mean arterial pressure nadir after administration of the 30- and 60-μg/kg doses of MK-467.
RESULTS Compared with baseline values, the dexmedetomidine infusion significantly decreased HR and increased arterial pressures. Each dose of MK-467 caused a significant decrease in arterial pressures and a significant, albeit clinically irrelevant, increase in HR (≤ 10%). Following administration of the 30- and 60-μg/kg doses of MK-467, all cats developed clinical hypotension (mean arterial pressure, < 60 mm Hg) even though CI and SVR returned to baseline values.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated administration of small doses of MK-467 to isoflurane-anesthetized cats receiving dexmedetomidine restored CI and SVR, but caused a substantial decrease in arterial pressures and only a marginal increase in HR. Therefore, caution should be used when MK-467 is administered to alleviate dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats.