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in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

Objective

To evaluate the sedative properties of 3 dosages of the benzodiazepine tranquilizer midazolam as a means of chemical restraint in quail (Colinus virginianus) and to evaluate the ability of the benzodiazepine antagonist flumazenil to reverse the sedative effects of midazolam

Design

Prospective randomized controlled trial

Animals

Study 1, 30 birds; study 2, 10 birds.

Procedure

2 studies were performed. In the first study, 30 birds were randomly assigned to receive midazolam at a dosage of 2, 4, or 6 mg/kg of body weight (10 birds/dosage). Degree of sedation was evaluated by use of a numerical scale, and the peak time of adequate chemical restraint was determined. The dosage in study 1 that produced the highest degree of sedation was administered to 10 birds in study 2. Flumazenil was administered at a dosage of 0.1 mg/ kg at the peak time of sedation that had been determined in study 1.

Results

Administration of 6 mg of midazolam/kg induced the highest degree of chemical restraint without causing alterations in cardiopulmonary function. Peak time of sedation was 10 minutes after administration; however, administration of 4 mg of midazolam/ kg also induced a high degree of sedation, but for a shorter period. Administration of flumazenil caused complete recovery from sedation induced with midazolam.

Clinical Implications

Administration of midazolam to wild birds induced adequate sedation. Results of the study reported here may be extrapolated to other species of wild birds, including raptors and, possibly, pet birds. (J Am Vet Med Assoc 1996;209:969-971)

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the α2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, α- adrenoceptor antagonists, were administered to isolate α1- or α2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/ kg of body weight, iv) and esmolol (50 to 75 μg/kg/ min, iv) to induce parasympathetic and β1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10−9 M) to 25.7 mg (10−4 M) and medetomidine (n = 3), 0.000237 mg (10−9 M) to 2.37 mg (10−5 M) after parasympathetic and β1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, iv) or medetomidine (n = 6, 0.05 mg/kg, iv) after parasympathetic and β1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, iv) followed by atipamezole (0.3 mg/kg, iv). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine.

Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause signficant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the α-adrenoceptor antagonists, prazosin (α1) and atipamezole (α2), did not cause significant changes in supraventricular or ventricular rate. α2-Adrenoceptor agonists do not induce direct α1- or α2-adrenoceptor-mediated depression of supraventricular or ventricular rate in dogs with complete atrioventricular block.

Free access
in American Journal of Veterinary Research