α2-Adrenergic receptor agonist effects on supraventricular and ventricular automaticity in dogs with complete atrioventricular block

Thomas K. Day From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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William W. Muir III From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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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 (10−9M) to 25.7 mg (10−4M) and medetomidine (n = 3), 0.000237 mg (10−9M) to 2.37 mg (10−5M) 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.

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 (10−9M) to 25.7 mg (10−4M) and medetomidine (n = 3), 0.000237 mg (10−9M) to 2.37 mg (10−5M) 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.

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