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- Author or Editor: Angela Briganti x
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Abstract
OBJECTIVE
To assess the effect of rocuronium bromide–induced mydriasis on the intraocular pressure (IOP) of kestrels (Falco tinnunculus) and little owls (Athene noctuae).
ANIMALS
13 adult kestrels and 13 adult little owls.
PROCEDURES
All birds were ophthalmologically normal. During the first of 2 treatment periods, a 1% rocuronium bromide solution was topically instilled in both eyes of all birds at a dose of 0.12 mg (12 μL) for kestrels and 0.20 mg (20 μL) for little owls. No ophthalmic treatments were administered during the second (control) treatment period, which was conducted 1 week after the first. During both treatment periods, rebound tonometry was used to measure IOP before rocuronium bromide instillation or at the beginning of the control period (baseline) and at predetermined times after baseline or until the pupillary light reflex returned to normal. All IOP measurements were obtained between 8 am and 5 pm.
RESULTS
The mean IOP did not differ significantly from baseline for either species during the control treatment period. During the rocuronium bromide treatment period, complete mydriasis was achieved in all birds. The mean IOP was significantly decreased from baseline and from the corresponding mean IOP for the control period beginning 60 and 30 minutes after drug instillation for kestrels and owls, respectively, and reached its nadir at 60 minutes after drug instillation for both species.
CONCLUSIONS AND CLINICAL RELEVANCE
Results indicated that topical instillation of rocuronium bromide in the eyes successfully induced mydriasis and decreased the IOP of common kestrels and little owls.
Abstract
Objective—To evaluate the pharmacokinetics and pharmacodynamics of zolpidem after oral administration of a single dose (0.15 or 0.50 mg/kg) and assess any associated antianxiety and sedative effects in dogs.
Animals—8 clinically normal sexually intact male dogs of various breeds.
Procedures—Dogs were assigned to 2 groups (4 dogs/group) and administered zolpidem orally once at a dose of 0.15 or 0.50 mg/kg in a crossover study; each dog received the other treatment once after an interval of 1 week. Blood samples were collected before and at intervals during the 24-hour period following dose administration. For each time point, plasma zolpidem concentration was evaluated via a validated method of high-performance liquid chromatography coupled with fluorescence detection, and pharmacodynamics were assessed via subjective assessments of sedation and level of agitation and selected clinical variables.
Results—The pharmacokinetic profile of zolpidem in dogs was dose dependent, and the plasma drug concentrations attained were lower than those for humans administered equivalent doses. The lower dose did not result in any clinical or adverse effects, but the higher dose generated paradoxical CNS stimulation of approximately 1 hour's duration and a subsequent short phase of mild sedation. This sedation phase was not considered to be of clinical relevance. The desired clinical effects were not evident at plasma zolpidem concentrations ≤ 30 ng/mL, and the minimal plasma concentration that induced adverse effects was 60 ng/mL.
Conclusions and Clinical Relevance—Results indicated that zolpidem is not a suitable drug for inducing sedation in dogs.
