Comparison of the effects of detomidine and xylazine on some α2-adrenoceptor-mediated responses in the central and peripheral nervous systems

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Abstract

The effects of detomidine, a novel veterinary sedative analgesic, on some ga2-adrenoceptor-mediated responses in the central and peripheral nervous systems were studied. In pithed rats, detomidine was a very potent agonist at both pre- and postsynaptic α2-adrenoceptors. Doses of 1.9 μg/kg and 6.5 μg/kg inhibited electrically induced tachycardia by 50% and increased mean blood pressure by 50 mmHg, respectively. In comparison, xylazine, though similar in specificity, was 40 times less potent than detomidine in this preparation. In unanaesthetized rats, detomidine both caused sedation and induced complex changes in body temperature. Low doses caused decreases in rectal temperature but these were reversed at the dose was increased. The decrease in rectal temperature could be blocked by yohimbine. Prazosin somewhat inhibited but did not eliminate the hyperthimia seen with the very high doses of detomidine. Xylazine caused much more severe falls in rectal temperature which could not be completely antagonized by α2-adrenoceptor blockade. Both detomidine and xylazine caused dose-dependent mydriasis in anaesthetized rats, detomidine being about 10 times more potent than xylazine. The mydriatic effects of detomidine could be prevented by α2- but not by α1-adrenoceptor blockade. It is concluded that detomidine is a potent and rather specific α2-adrenoceptor agonist in the central and peripheral nervous systems. In comparison with xylazine, detomidine has higher potency and greater specificity, especially at central α2-adrenoceptors.

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